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Buytaert M, Declercq D, Depoorter F, Cosijn Z, Devisscher L, Raevens S, Verhelst X, Van Vlierberghe H, Geerts A, De Bruyne R, Lefere S. The association of ultra-processed food intake with adolescent metabolic dysfunction-associated steatotic liver disease in the NHANES. Pediatr Obes 2025; 20:e13174. [PMID: 39340247 DOI: 10.1111/ijpo.13174] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/26/2024] [Revised: 08/01/2024] [Accepted: 08/26/2024] [Indexed: 09/30/2024]
Abstract
INTRODUCTION Metabolic dysfunction-associated steatotic liver disease (MASLD) has become a major public health concern. A thorough analysis of the link between ultra-processed food (UPF) intake and MASLD in the adolescent population is lacking. METHODS Adolescent participants of the National Health and Nutrition Examination Survey (NHANES) pre-pandemic cohort were included. Different controlled attenuation parameter (CAP) cut-offs were used to assess MASLD. The percentage energy intake of UPF, categorized according to the NOVA classification, to total energy intake was taken as the main outcome marker. Structural equation modelling (SEM) was used to better quantify the causal connection between UPF and liver steatosis. RESULTS UPF consumption constituted a median 75% (62-86) of total energy intake. There was no significant correlation between UPF intake and CAP (ρ = 0.061, p = 0.091). The median proportion UPF intake was not associated with steatosis severity. SEM similarly yielded a weak and non-significant correlation of 0.078. In participants with MASLD, total energy intake was significantly higher (p < 0.001) and sugar-containing beverage (SCB) consumption showed a non-significant trend towards higher consumption. CONCLUSIONS No clinically relevant association between UPF intake and MASLD in adolescents could be demonstrated. Our results nonetheless suggest that total energy intake and consumption of SCBs are important contributors to paediatric obesity and MASLD.
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Affiliation(s)
- Maarten Buytaert
- Department of Internal Medicine and Pediatrics, Hepatology Research Unit, Ghent University, Ghent, Belgium
- Liver Research Center Ghent, Ghent University Hospital, Ghent, Belgium
| | - Dimitri Declercq
- Department of Internal Medicine and Pediatrics, Ghent University, Ghent, Belgium
- Center for Nutrition and Dietetics, Ghent University Hospital, Ghent, Belgium
| | - Fleur Depoorter
- Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium
| | - Zerlina Cosijn
- Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium
| | - Lindsey Devisscher
- Liver Research Center Ghent, Ghent University Hospital, Ghent, Belgium
- Department of Basic and Applied Medical Sciences, Gut-Liver Immunopharmacology Unit, Ghent University, Ghent, Belgium
| | - Sarah Raevens
- Department of Internal Medicine and Pediatrics, Hepatology Research Unit, Ghent University, Ghent, Belgium
- Liver Research Center Ghent, Ghent University Hospital, Ghent, Belgium
| | - Xavier Verhelst
- Department of Internal Medicine and Pediatrics, Hepatology Research Unit, Ghent University, Ghent, Belgium
- Liver Research Center Ghent, Ghent University Hospital, Ghent, Belgium
| | - Hans Van Vlierberghe
- Department of Internal Medicine and Pediatrics, Hepatology Research Unit, Ghent University, Ghent, Belgium
- Liver Research Center Ghent, Ghent University Hospital, Ghent, Belgium
| | - Anja Geerts
- Department of Internal Medicine and Pediatrics, Hepatology Research Unit, Ghent University, Ghent, Belgium
- Liver Research Center Ghent, Ghent University Hospital, Ghent, Belgium
| | - Ruth De Bruyne
- Liver Research Center Ghent, Ghent University Hospital, Ghent, Belgium
- Department of Pediatric Gastroenterology, Hepatology and Nutrition, Ghent University Hospital, Ghent, Belgium
| | - Sander Lefere
- Department of Internal Medicine and Pediatrics, Hepatology Research Unit, Ghent University, Ghent, Belgium
- Liver Research Center Ghent, Ghent University Hospital, Ghent, Belgium
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Faienza MF, Baima J, Cecere V, Monteduro M, Farella I, Vitale R, Antoniotti V, Urbano F, Tini S, Lenzi FR, Prodam F. Fructose Intake and Unhealthy Eating Habits Are Associated with MASLD in Pediatric Obesity: A Cross-Sectional Pilot Study. Nutrients 2025; 17:631. [PMID: 40004960 PMCID: PMC11858415 DOI: 10.3390/nu17040631] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/30/2025] [Revised: 02/06/2025] [Accepted: 02/09/2025] [Indexed: 02/27/2025] Open
Abstract
Background/Objectives: Fructose consumption in children is increasing, as is the prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD). Despite evidence linking added sugars to metabolic syndrome, fructose's impact on liver disease in youth remains unclear, especially in pediatrics. Our study aimed to evaluate the role of fructose intake in metabolic and liver dysfunction in a cohort of pre-school children and adolescents with obesity. Methods: We recruited 41 children and adolescents with obesity (age range: 2.5-16 years, BMI SDS 2.6 ± 0.5 kg/m2). Clinical and biochemical parameters were assessed. Through ultrasound (US), MASLD, hepatorenal index (HRI), subcutaneous adipose tissue (scAT), and visceral adipose tissue (vAT) were assessed. Dietary intake was evaluated using the IDEFICS FFQ and a fructose-specific questionnaire. Results: Pubertal subjects had more scAT and vAT, higher insulin resistance, and higher liver fibrosis parameters than those prepubertal. MASLD was detected in 12 subjects, associated with higher scAT and vAT. Pubertal subjects had lower weekly fructose intake than prepubertal subjects (p < 0.02). However, they consumed less fructose from fruits (p < 0.04) and more from other sugars (p < 0.04) than younger children. Patients with MASLD reported higher fructose intake (p < 0.01), primarily from fruits (p < 0.003), likely due to misreporting, alongside higher consumption of unhealthy food, mainly rich in saturated fats. Conclusions: Fructose intake and unhealthy dietary habits were associated with MASLD in pre-school and adolescents with obesity. Advice to pay attention to fructose intake and foods rich in saturated fats is mandatory to decrease both obesity and MASLD. Further high-powered studies in any pediatric age and different geographical areas are needed to better evaluate the MASLD history.
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Affiliation(s)
- Maria Felicia Faienza
- Pediatric Unit, Department of Precision and Regenerative Medicine and Ionian Area, University of Bari “A. Moro”, 70124 Bari, Italy;
| | - Jessica Baima
- Unit of Endocrinology, Department of Health Sciences, University of Piemonte Orientale, 28100 Novara, Italy; (J.B.); (V.A.); (S.T.)
| | - Valentina Cecere
- Giovanni XXIII Pediatric Hospital, University of Bari “A. Moro”, 70124 Bari, Italy; (V.C.); (R.V.); (F.U.)
| | | | - Ilaria Farella
- Department of Medicine and Surgery, LUM University, 70010 Casamassima, Italy;
| | - Rossella Vitale
- Giovanni XXIII Pediatric Hospital, University of Bari “A. Moro”, 70124 Bari, Italy; (V.C.); (R.V.); (F.U.)
| | - Valentina Antoniotti
- Unit of Endocrinology, Department of Health Sciences, University of Piemonte Orientale, 28100 Novara, Italy; (J.B.); (V.A.); (S.T.)
| | - Flavia Urbano
- Giovanni XXIII Pediatric Hospital, University of Bari “A. Moro”, 70124 Bari, Italy; (V.C.); (R.V.); (F.U.)
| | - Sabrina Tini
- Unit of Endocrinology, Department of Health Sciences, University of Piemonte Orientale, 28100 Novara, Italy; (J.B.); (V.A.); (S.T.)
| | - Francesca Romana Lenzi
- Laboratory of Psychology and Social Processes in Sport, Department of Movement, Human and Health Sciences, University of Rome “Foro Italico”, 00135 Rome, Italy;
| | - Flavia Prodam
- Unit of Endocrinology, Department of Health Sciences, University of Piemonte Orientale, 28100 Novara, Italy; (J.B.); (V.A.); (S.T.)
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Zhao G, Chondon S, Gray C, Gentili S, Stanley M, Regnault TRH. Fructose Consumption in Pregnancy and Associations with Maternal and Offspring Hepatic and Whole-Body Adiposity in Rodents: A Scoping Review. Curr Dev Nutr 2025; 9:104510. [PMID: 39896731 PMCID: PMC11782591 DOI: 10.1016/j.cdnut.2024.104510] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/19/2024] [Revised: 11/01/2024] [Accepted: 11/10/2024] [Indexed: 02/04/2025] Open
Abstract
Background Excess fructose consumption has been linked to adverse metabolic health, including impaired hepatic function and increased adiposity. The early life period, including preconception, pregnancy, and the newborn period, are critical periods in determining later metabolic health. However, the impact of excess fructose intake during this time on maternal, fetal, and offspring hepatic and whole-body adiposity, is not well defined. Objectives To understand the effects of maternal fructose consumption pre- and during pregnancy on maternal, fetal, and offspring hepatic and whole-body adiposity. Methods A systematic search of MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials was performed up to October 4, 2024, to identify animal and human studies that focused on maternal fructose consumption pre- and during pregnancy on hepatic and whole-body adiposity in the mother, fetus, and offspring. Citations, abstracts, and full texts were screened in duplicate. Hepatic adiposity was defined as elevated hepatic triglycerides or overall hepatic lipid accumulation. Whole-body adiposity was defined as increased adipose tissue, serum lipids, or adipocyte hypertrophy. Results After screening 2538 citations, 37 experimental rodent studies reporting maternal fructose consumption pre- and during pregnancy in rodents were included. No human studies met the inclusion criteria. Prenatal fructose exposure was associated with maternal (9 of 12) and offspring (7 of 11) whole-body adiposity. A high proportion of studies (13 of 14) supported the association between fructose during pregnancy and increased maternal hepatic adiposity. Fetal hepatic adiposity and elevated expression of hepatic lipogenic proteins were noted in 4 studies. Offspring hepatic adiposity was supported in 16 of the 20 articles that discussed hepatic results, with 5 studies demonstrating more severe effects in female offspring. Conclusions Fructose consumption during pregnancy in rodent models is associated with maternal, fetal, and offspring hepatic and whole-body adiposity with underlying sex-specific effects. No human studies met the inclusion criteria. Registration number H8F26 on Open Science Framework (https://doi.org/10.17605/OSF.IO/H8F26).
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Affiliation(s)
- Grace Zhao
- Department of Obstetrics and Gynaecology, Western University, London, ON, Canada
| | - Sarah Chondon
- Department of Obstetrics and Gynaecology, Schulich School of Medicine, Western University, London, ON, Canada
| | - Clint Gray
- Gillies McIndoe Research Institute, New Zealand
- Department of Paediatrics & Child Health, University of Otago, New Zealand
| | - Sheridan Gentili
- Teaching Innovation Unit, University of South Australia, Australia
| | - Meagan Stanley
- Western Libraries, Western University, London, ON, Canada
| | - Timothy RH Regnault
- Department of Obstetrics and Gynaecology, Western University, London, ON, Canada
- Department of Physiology and Pharmacology, Western University, London, ON, Canada
- Division of Maternal, Fetal, and Newborn Health, Children’s Health Research Institute, London, ON, Canada
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Baharuddin B. The Impact of Fructose Consumption on Human Health: Effects on Obesity, Hyperglycemia, Diabetes, Uric Acid, and Oxidative Stress With a Focus on the Liver. Cureus 2024; 16:e70095. [PMID: 39355469 PMCID: PMC11444807 DOI: 10.7759/cureus.70095] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 09/24/2024] [Indexed: 10/03/2024] Open
Abstract
Excessive fructose consumption, primarily through processed foods and beverages, has become a significant public health concern due to its association with various metabolic disorders. This review examines the impact of fructose on human health, focusing on its role in obesity, insulin resistance, hyperglycemia, type 2 diabetes, uric acid production, and oxidative stress. Fructose metabolism, distinct from glucose, predominantly occurs in the liver, where it bypasses normal insulin regulation, leading to increased fat synthesis through de novo lipogenesis. This process contributes to the development of non-alcoholic fatty liver disease and elevates the risk of cardiovascular disease. Furthermore, fructose-induced adenosine triphosphate depletion activates purine degradation, increasing uric acid levels and exacerbating hyperuricemia. The overproduction of reactive oxygen species during fructose metabolism also drives oxidative stress, promoting inflammation and cellular damage. By synthesizing recent findings, this review underscores the importance of regulating fructose intake, implementing public health policies, and adopting lifestyle changes to mitigate these adverse effects.
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Vargas-Vargas MA, González-Montoya M, Torres-Isidro O, García-Berumen CI, Ortiz-Avila O, Calderón-Cortés E, Cortés-Rojo C. Assessing the impact of concurrent high-fructose and high-saturated fat diets on pediatric metabolic syndrome: A review. World J Clin Pediatr 2024; 13:91478. [PMID: 38947987 PMCID: PMC11212767 DOI: 10.5409/wjcp.v13.i2.91478] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/29/2023] [Revised: 04/22/2024] [Accepted: 05/06/2024] [Indexed: 06/07/2024] Open
Abstract
High-saturated fat (HF) or high-fructose (HFr) consumption in children predispose them to metabolic syndrome (MetS). In rodent models of MetS, diets containing individually HF or HFr lead to a variable degree of MetS. Nevertheless, simultaneous intake of HF plus HFr have synergistic effects, worsening MetS outcomes. In children, the effects of HF or HFr intake usually have been addressed individually. Therefore, we have reviewed the outcomes of HF or HFr diets in children, and we compare them with the effects reported in rodents. In humans, HFr intake causes increased lipogenesis, hypertriglyceridemia, obesity and insulin resistance. On the other hand, HF diets promote low grade-inflammation, obesity, insulin resistance. Despite the deleterious effects of simultaneous HF plus HFr intake on MetS development in rodents, there is little information about the combined effects of HF plus HFr intake in children. The aim of this review is to warn about this issue, as individually addressing the effects produced by HF or HFr may underestimate the severity of the outcomes of Western diet intake in the pediatric population. We consider that this is an alarming issue that needs to be assessed, as the simultaneous intake of HF plus HFr is common on fast food menus.
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Affiliation(s)
- Manuel Alejandro Vargas-Vargas
- Instituto de Investigaciones Químico – Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia 58030, Michoacán, Mexico
| | - Marcela González-Montoya
- Instituto de Investigaciones Químico – Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia 58030, Michoacán, Mexico
| | - Olin Torres-Isidro
- Instituto de Investigaciones Químico – Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia 58030, Michoacán, Mexico
| | - Claudia Isabel García-Berumen
- Instituto de Investigaciones Químico – Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia 58030, Michoacán, Mexico
| | - Omar Ortiz-Avila
- Facultad de Enfermería, Universidad Michoacana de San Nicolás de Hidalgo, Morelia 58020, Michoacán, Mexico
| | - Elizabeth Calderón-Cortés
- Facultad de Enfermería, Universidad Michoacana de San Nicolás de Hidalgo, Morelia 58020, Michoacán, Mexico
| | - Christian Cortés-Rojo
- Instituto de Investigaciones Químico – Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia 58030, Michoacán, Mexico
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Distefano JK, Gerhard GS. Effects of dietary sugar restriction on hepatic fat in youth with obesity. Minerva Pediatr (Torino) 2024; 76:439-448. [PMID: 37284808 PMCID: PMC11229704 DOI: 10.23736/s2724-5276.23.07209-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 06/08/2023]
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in children. Like adults, children can develop the progressive form of NAFLD, nonalcoholic steatohepatitis (NASH), which is characterized by hepatic inflammation, often in the presence of fibrosis. Children with NAFLD are at higher risk of liver-related complications, metabolic dysfunction, and cardiovascular disease in adulthood. Many factors contribute to the escalating prevalence of NAFLD in the pediatric population, among which are an array of dietary patterns such as overnutrition, poor diet quality, and heavy consumption of fat and sugar, including fructose. Findings from an increasing number of epidemiological studies support a connection between high habitual sugar consumption and NAFLD, especially within the context of obesity, but these studies are not able to demonstrate whether sugar is a contributing factor or instead an indicator of an overall poor diet (or lifestyle) quality. To date, only four randomized controlled dietary interventions assessing the effects of sucrose/fructose restriction on hepatic fat fraction in youth with obesity have been published. The objectives of this review are to summarize the key findings from these dietary interventions to achieve a better understanding of the strength of the relationship between dietary sugar restriction and liver fat reduction, despite their inherent limitations, and to discuss the potential impact of weight loss and fat mass reduction on improvement in hepatic steatosis.
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Affiliation(s)
- Johanna K Distefano
- Metabolic Disease Research Unit, Translational Genomics Research Institute, Phoenix, AZ, USA -
| | - Glenn S Gerhard
- Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA, USA
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Lee EH, Kim JY, Yang HR. Sex-specific differences in ectopic fat and metabolic characteristics of paediatric nonalcoholic fatty liver disease. Int J Obes (Lond) 2024; 48:486-494. [PMID: 38114813 DOI: 10.1038/s41366-023-01439-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/03/2023] [Revised: 11/22/2023] [Accepted: 12/01/2023] [Indexed: 12/21/2023]
Abstract
BACKGROUND/OBJECTIVES Sex-specific differences in obesity-related metabolic characteristics of non-alcoholic fatty liver disease (NAFLD) have rarely been explored, particularly in children with biopsy-verified NAFLD. The influence of sex hormones on ectopic fat disposition may cause inter-sex differences in various metabolic factors. This study aimed to assess the sex-based differences in ectopic fat and metabolic characteristics in children with NAFLD. SUBJECT/METHODS We enrolled 63 children with biopsy-verified NAFLD (48 boys; mean age, 12.9 ± 3.2 years; mean body mass index z-score [BMI-z], 2.49 ± 1.21). Ectopic fat in the liver and pancreas was quantified based on magnetic resonance imaging within 2 days of the liver biopsy. Laboratory tests, body composition, blood pressure, and anthropometric measurements were also assessed. RESULTS Sex-based differences were neither observed in age, BMI-z, or total body fat percentage nor in the proportions of obesity, abdominal obesity, diabetes, dyslipidaemia, hypertension, or metabolic syndrome. Furthermore, liver enzyme levels, lipid profiles, and pancreatic fat did not differ between the sexes. However, boys had significantly higher fasting insulin (median 133.2 vs. 97.8 pmol/L; p = 0.039), fasting plasma glucose (median 5.30 vs. 4.83 mmol/L; p = 0.013), homeostasis model assessment of insulin resistance (median 5.4 vs. 3.6; p = 0.025), serum uric acid (404.1 ± 101.2 vs. 322.4 ± 87.1 μmol/L; p = 0.009), and liver fat (median 26.3% vs. 16.3%; p = 0.014). CONCLUSIONS Male-predominant hepatic steatosis and insulin resistance caused by sex-specific ectopic fat accumulation may contribute to higher uric acid levels in boys than in girls with NAFLD.
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Affiliation(s)
- Eun Hye Lee
- Department of Pediatrics, Nowon Eulji Medical Center, Eulji University School of Medicine, Seoul, South Korea
| | - Ji Young Kim
- Department of Radiology, Seoul National University Bundang Hospital, Seongnam, South Korea
| | - Hye Ran Yang
- Department of Pediatrics, Seoul National University Bundang Hospital, Seongnam, South Korea.
- Department of Pediatrics, Seoul National University College of Medicine, Seoul, South Korea.
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de Cuevillas B, Lubrecht J, Navas-Carretero S, Vreugdenhil A, Martinez JA. Sleep duration is associated with liver steatosis in children depending on body adiposity. Eur J Pediatr 2024; 183:779-789. [PMID: 38001309 PMCID: PMC10912132 DOI: 10.1007/s00431-023-05332-2] [Citation(s) in RCA: 1] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/01/2023] [Revised: 11/03/2023] [Accepted: 11/08/2023] [Indexed: 11/26/2023]
Abstract
Sleep is a factor associated with overweight/obesity risk, wherein interactions with fatty liver should be ascertained. The aim of this cross-sectional study was to analyze the possible relationships of sleep with liver health and whether this interplay is related to body adiposity distribution in children and adolescents. Anthropometric, clinical, and biochemical measurements were performed in children and adolescents (2-18 years old) with overweight/obesity (n = 854). Body fat distribution was clinically assessed, and several hepatic markers, including hepatic steatosis index, were calculated. Sleep time mediation (hours/day) in the relationship between the hepatic steatosis index and body fat distribution was investigated. Differences among diverse fatty liver disease scores were found between children with overweight or obesity (p < 0.05). Linear regression models showed associations between hepatic steatosis index and lifestyle markers (p < 0.001). Hepatic steatosis index was higher (about + 15%) in children with obesity compared to overweight (p < 0.001). Pear-shaped body fat distribution may seemingly play a more detrimental role on liver fat deposition. The association between sleep time and hepatic steatosis index was dependent on body mass index z-score. Post hoc analyses showed that 39% of the relationship of body fat distribution on hepatic steatosis index may be explained by sleep time. Conclusion: An association of sleep time in the relationship between body fat distribution and hepatic steatosis index was observed in children and adolescents with overweight/obesity, which can be relevant in the prevention and treatment of excessive adiposity between 2 and 18 years old. CLINICAL TRIAL NCT04805762. Import: As part of a healthy lifestyle, sleep duration might be a modifiable factor in the management of fatty liver disease in children. WHAT IS KNOWN • Sleep is an influential factor of overweight and obesity in children. • Excessive adiposity is associated with liver status in children and adolescents. WHAT IS NEW • Sleep time plays a role in the relationship between body fat distribution and liver disease. • Monitoring sleep pattern may be beneficial in the treatment of hepatic steatosis in children with excessive body weight.
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Affiliation(s)
- Begoña de Cuevillas
- Center for Nutrition Research, Department of Nutrition, Food Sciences and Physiology, School of Pharmacy and Nutrition, University of Navarra, Irunlarrea 1, 31008, Pamplona, Spain.
| | - Judith Lubrecht
- Department of Pediatrics, Maastricht University Medical Centre, Maastricht, The Netherlands
- School of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, Maastricht, The Netherlands
| | - Santiago Navas-Carretero
- Center for Nutrition Research, Department of Nutrition, Food Sciences and Physiology, School of Pharmacy and Nutrition, University of Navarra, Irunlarrea 1, 31008, Pamplona, Spain
- Centro de Investigación Biomédica en Red de la Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain
- IdiSNA, Health Research Institute of Navarra, Pamplona, Spain
| | - Anita Vreugdenhil
- Department of Pediatrics, Maastricht University Medical Centre, Maastricht, The Netherlands
- School of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, Maastricht, The Netherlands
| | - J Alfredo Martinez
- Center for Nutrition Research, Department of Nutrition, Food Sciences and Physiology, School of Pharmacy and Nutrition, University of Navarra, Irunlarrea 1, 31008, Pamplona, Spain
- Centro de Investigación Biomédica en Red de la Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Madrid, Spain
- Precision Nutrition Program, Research Institute On Food and Health Sciences IMDEA Food, CSIC-UAM, Madrid, Spain
- Centro de Medicina y Endocrinología, Universidad de Valladolid, Valladolid, Spain
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Gong P, Long H, Guo Y, Wang Z, Yao W, Wang J, Yang W, Li N, Xie J, Chen F. Chinese herbal medicines: The modulator of nonalcoholic fatty liver disease targeting oxidative stress. JOURNAL OF ETHNOPHARMACOLOGY 2024; 318:116927. [PMID: 37532073 DOI: 10.1016/j.jep.2023.116927] [Citation(s) in RCA: 19] [Impact Index Per Article: 19.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 02/27/2023] [Revised: 07/05/2023] [Accepted: 07/14/2023] [Indexed: 08/04/2023]
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE Plants are a natural treasure trove; their secondary metabolites participate in several pharmacological processes, making them a crucial component in the synthesis of novel pharmaceuticals and serving as a reserve resource foundation in this process. Nonalcoholic fatty liver disease (NAFLD) is associated with the risk of progression to hepatitis and liver cancer. The "Treatise on Febrile Diseases," "Compendium of Materia Medica," and "Thousand Golden Prescriptions" have listed herbal remedies to treat liver diseases. AIM OF THE REVIEW Chinese herbal medicines have been widely used for the prevention and treatment of NAFLD owing to their efficacy and low side effects. The production of reactive oxygen species (ROS) during NAFLD, and the impact and potential mechanism of ROS on the pathogenesis of NAFLD are discussed in this review. Furthermore, common foods and herbs that can be used to prevent NAFLD, as well as the structure-activity relationships and potential mechanisms, are discussed. METHODS Web of Science, PubMed, CNKI database, Google Scholar, and WanFang database were searched for natural products that have been used to treat or prevent NAFLD in the past five years. The primary search was performed using the following keywords in different combinations in full articles: NAFLD, herb, natural products, medicine, and ROS. More than 400 research papers and review articles were found and analyzed in this review. RESULTS By classifying and discussing the literature, we obtained 86 herbaceous plants, 28 of which were derived from food and 58 from Chinese herbal medicines. The mechanism of NAFLD was proposed through experimental studies on thirteen natural compounds (quercetin, hesperidin, rutin, curcumin, resveratrol, epigallocatechin-3-gallate, salvianolic acid B, paeoniflorin, ginsenoside Rg1, ursolic acid, berberine, honokiol, emodin). The occurrence and progression of NAFLD could be prevented by natural antioxidants through several pathways to prevent ROS accumulation and reduce hepatic cell injuries caused by excessive ROS. CONCLUSION This review summarizes the natural products and routinely used herbs (prescription) in the prevention and treatment of NAFLD. Firstly, the mechanisms by which natural products improve NAFLD through antioxidant pathways are elucidated. Secondly, the potential of traditional Chinese medicine theory in improving NAFLD is discussed, highlighting the safety of food-medicine homology and the broader clinical potential of multi-component formulations in improving NAFLD. Aiming to provide theoretical basis for the prevention and treatment of NAFLD.
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Affiliation(s)
- Pin Gong
- School of Food and Biotechnological Engineering, Shaanxi University of Science and Technology, Xi'an, 710021, China
| | - Hui Long
- School of Food and Biotechnological Engineering, Shaanxi University of Science and Technology, Xi'an, 710021, China
| | - Yuxi Guo
- School of Food and Biotechnological Engineering, Shaanxi University of Science and Technology, Xi'an, 710021, China
| | - Zhineng Wang
- School of Food and Biotechnological Engineering, Shaanxi University of Science and Technology, Xi'an, 710021, China
| | - Wenbo Yao
- School of Food and Biotechnological Engineering, Shaanxi University of Science and Technology, Xi'an, 710021, China
| | - Jing Wang
- School of Food and Biotechnological Engineering, Shaanxi University of Science and Technology, Xi'an, 710021, China
| | - Wenjuan Yang
- School of Food and Biotechnological Engineering, Shaanxi University of Science and Technology, Xi'an, 710021, China
| | - Nan Li
- School of Food and Biotechnological Engineering, Shaanxi University of Science and Technology, Xi'an, 710021, China
| | - Jianwu Xie
- School of Food and Biotechnological Engineering, Shaanxi University of Science and Technology, Xi'an, 710021, China.
| | - Fuxin Chen
- School of Chemistry and Chemical Engineering, Xi'an University of Science and Technology, Xi'an, 710054, China.
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Smiliotopoulos T, Zampelas A, Houliaras G, Sgouros SN, Michas G, Bamias G, Panagiotakos D, Cholopoulos N, Chrousos GP, Roma E, Magriplis E. Association of fructose consumption with prevalence of functional gastrointestinal disorders manifestations: results from Hellenic National Nutrition and Health Survey (HNNHS). Br J Nutr 2023; 130:1961-1972. [PMID: 37197939 PMCID: PMC10630147 DOI: 10.1017/s0007114523001198] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/22/2022] [Revised: 05/02/2023] [Accepted: 05/09/2023] [Indexed: 05/19/2023]
Abstract
The study aimed to assess the total prevalence of functional gastrointestinal disorders (FGID), and separately, irritable bowel syndrome (IBS) among adults and to determine their potential association with fructose consumption. Data from the Hellenic National Nutrition and Health Survey were included (3798 adults; 58·9 % females). Information regarding FGID symptomatology was assessed using self-reported physician diagnosis questionnaires the reliability of which were screened using the ROME III, in a sample of the population. Fructose intake was estimated from 24 h recalls, and the MedDiet score was used to assess adherence to the Mediterranean diet. The prevalence of FGID symptomatology was 20·2 %, while 8·2 % had IBS (representing 40·2 % of total FGID). The likelihood of FGID was 28 % higher (95 %CI: 1·03-1·6) and of IBS 49 % (95 %CI: 1·08-2·05) in individuals with higher fructose intake than with lower intake (3rd tertile compared with 1st). When area of residence was accounted for, individuals residing in the Greek islands had a significantly lower probability of FGID and IBS compared with those residing in Mainland and the main Metropolitan areas, with Islanders also achieving a higher MedDiet score and lower added sugar intake, comparatively to inhabitants of the main metropolitan areas. FGID and IBS symptomatology was most prominent among individuals with higher fructose consumption, and this was most conspicuous in areas with a lower Mediterranean diet adherence, suggesting that the dietary source of fructose rather than total fructose should be examined in relation to FGID.
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Affiliation(s)
- Theodoros Smiliotopoulos
- Laboratory of Dietetics and Quality of Life, Department of Food Science and Human Nutrition, Agricultural University of Athens, 11855Athens, Greece
| | - Antonis Zampelas
- Laboratory of Dietetics and Quality of Life, Department of Food Science and Human Nutrition, Agricultural University of Athens, 11855Athens, Greece
| | - George Houliaras
- First Department of Pediatrics, Medical School, National and Kapodistrian University of Athens, 11527Athens, Greece
| | - Spiros N. Sgouros
- Department of Gastroenterology, Athens Naval Hospital, 7011528Athens, Greece
| | - George Michas
- Laboratory of Dietetics and Quality of Life, Department of Food Science and Human Nutrition, Agricultural University of Athens, 11855Athens, Greece
| | - George Bamias
- Department of Gastroenterology, Athens Naval Hospital, 7011528Athens, Greece
| | - Demosthenes Panagiotakos
- Department of Nutrition and Dietetics, School of Health Science and Education Harokopio University, 17676Athens, Greece
| | - Nikolaos Cholopoulos
- Department of Medicine, School of Health Sciences, Aristotle University of Thessaloniki, University Campus, 54124Thessaloniki, Greece
| | - George P. Chrousos
- University Research Institute of Maternal and Child Health and Precision Medicine and UNESCO Chair on Adolescent Health Care, Medical School, National and Kapodistrian University of Athens, 11527Athens, Greece
| | - Eleftheria Roma
- First Department of Pediatrics, Medical School, National and Kapodistrian University of Athens, 11527Athens, Greece
| | - Emmanuella Magriplis
- Laboratory of Dietetics and Quality of Life, Department of Food Science and Human Nutrition, Agricultural University of Athens, 11855Athens, Greece
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11
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Orry S, Dalstrup Jakobsen D, Kristensen NM, Meldgaard Bruun J. Uric acid and sCD163 as biomarkers for metabolic dysfunction and MAFLD in children and adolescents with overweight and obesity. J Pediatr Endocrinol Metab 2023; 0:jpem-2023-0228. [PMID: 37285233 DOI: 10.1515/jpem-2023-0228] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/14/2023] [Accepted: 05/22/2023] [Indexed: 06/09/2023]
Abstract
OBJECTIVES The prevalence of childhood obesity increases globally, and noninvasive methods are needed to identify metabolic dysfunction and obesity-related complications such as pediatric metabolic associated fatty liver disease (MAFLD). We investigated whether uric acid (UA) and the macrophage marker soluble form of cysteine scavenger receptor CD163 (sCD163) can be used as biomarkers for deteriorated metabolism or pediatric MAFLD in children with overweight or obesity. METHODS Cross-sectional clinical and biochemical data from 94 children with overweight or obesity was included. Surrogate liver markers were calculated, and correlations were investigated using Pearson's or Spearman's correlation test. RESULTS UA and sCD163 correlated with BMI standard deviation score (r=0.23, p<0.05; r=0.33, p<0.01) and body fat (r=0.24, p<0.05; r=0.27, p=0.01). UA correlated with triglycerides (ρ=0.21, p<0.05), fat free mass (r=0.33, p<0.01), and gamma-glutamyl transferase (r=0.39, p<0.01). sCD163 correlated with the pediatric NAFLD fibrosis score (r=0.28, p<0.01) and alanine aminotransferase (r=0.28, p<0.01). No correlation was found between UA and pediatric MAFLD. CONCLUSIONS UA and sCD163 was identified as markers of a deranged metabolic profile, thus acting as easily accessible biomarkers for obesity and an obesity-related deranged metabolism. Furthermore, increasing levels of sCD163 could be a useful biomarker of pediatric MAFLD. Future prospective studies are warranted.
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Affiliation(s)
- Sofie Orry
- Steno Diabetes Center Aarhus, Aarhus University Hospital, Aarhus, Denmark
| | - Dorthe Dalstrup Jakobsen
- Steno Diabetes Center Aarhus, Aarhus University Hospital, Aarhus, Denmark
- Department of Clinical Medicine, University of Aarhus, Aarhus, Denmark
- Danish National Center for Obesity, Aarhus, Denmark
| | | | - Jens Meldgaard Bruun
- Steno Diabetes Center Aarhus, Aarhus University Hospital, Aarhus, Denmark
- Department of Clinical Medicine, University of Aarhus, Aarhus, Denmark
- Danish National Center for Obesity, Aarhus, Denmark
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12
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Klepper CM, Khurana T, Sun Q, Fei L, Crimmins NA, Siegel R, Mouzaki M. BMI Metrics Are Poor Predictors of Pediatric Nonalcoholic Fatty Liver Disease Severity. Child Obes 2023; 19:139-143. [PMID: 35475755 PMCID: PMC9986011 DOI: 10.1089/chi.2021.0316] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/13/2022]
Abstract
Background: Alternative BMI metrics are superior to BMI z score (BMIz) in tracking obesity but have not been evaluated in patients with nonalcoholic fatty liver disease (NAFLD). Our objective was to evaluate whether BMI-adjusted z score (BMIaz) or BMI expressed as a percentage of the 95th percentile (%BMIp95) are better predictors of degree of alanine aminotransferase (ALT) elevation, a surrogate for NAFLD severity, compared with BMIz in patients with NAFLD. Methods: A retrospective study of 776 subjects aged 2-18 years with BMIz > 1.0 followed in a NAFLD subspecialty clinic was conducted. Regression analysis was used to determine predictors of elevated ALT. Results: There was no association between BMIz, BMIaz, or %BMIp95 and degree of ALT elevation using linear or logistic regression. Conclusion: These results do not support the use of alternative BMI metrics for evaluating NAFLD severity. Future studies should investigate longitudinal assessments and correlation with histology.
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Affiliation(s)
- Corie M. Klepper
- Divisions of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA
| | - Tarush Khurana
- Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA
| | - Qin Sun
- Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA
- Divisions of Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA
| | - Lin Fei
- Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA
- Divisions of Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA
| | - Nancy A. Crimmins
- Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA
- Divisions of Endocrinology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA
| | - Robert Siegel
- Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA
- Divisions of Cardiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA
| | - Marialena Mouzaki
- Divisions of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA
- Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA
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13
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Petito G, Giacco A, Cioffi F, Mazzoli A, Magnacca N, Iossa S, Goglia F, Senese R, Lanni A. Short-term fructose feeding alters tissue metabolic pathways by modulating microRNAs expression both in young and adult rats. Front Cell Dev Biol 2023; 11:1101844. [PMID: 36875756 PMCID: PMC9977821 DOI: 10.3389/fcell.2023.1101844] [Citation(s) in RCA: 5] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/18/2022] [Accepted: 02/06/2023] [Indexed: 02/18/2023] Open
Abstract
Dietary high fructose (HFrD) is known as a metabolic disruptor contributing to the development of obesity, diabetes, and dyslipidemia. Children are more sensitive to sugar than adults due to the distinct metabolic profile, therefore it is especially relevant to study the metabolic alterations induced by HFrD and the mechanisms underlying such changes in animal models of different ages. Emerging research suggests the fundamental role of epigenetic factors such as microRNAs (miRNAs) in metabolic tissue injury. In this perspective, the aim of the present study was to investigate the involvement of miR-122-5p, miR-34a-5p, and miR-125b-5p examining the effects induced by fructose overconsumption and to evaluate whether a differential miRNA regulation exists between young and adult animals. We used young rats (30 days) and adult rats (90 days) fed on HFrD for a short period (2 weeks) as animal models. The results indicate that both young and adult rats fed on HFrD exhibit an increase in systemic oxidative stress, the establishment of an inflammatory state, and metabolic perturbations involving the relevant miRNAs and their axes. In the skeletal muscle of adult rats, HFrD impair insulin sensitivity and triglyceride accumulation affecting the miR-122-5p/PTP1B/P-IRS-1(Tyr612) axis. In liver and skeletal muscle, HFrD acts on miR-34a-5p/SIRT-1: AMPK pathway resulting in a decrease of fat oxidation and an increase in fat synthesis. In addition, liver and skeletal muscle of young and adult rats exhibit an imbalance in antioxidant enzyme. Finally, HFrD modulates miR-125b-5p expression levels in liver and white adipose tissue determining modifications in de novo lipogenesis. Therefore, miRNA modulation displays a specific tissue trend indicative of a regulatory network that contributes in targeting genes of various pathways, subsequently yielding extensive effects on cell metabolism.
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Affiliation(s)
- Giuseppe Petito
- Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, University of Campania "L. Vanvitelli", Caserta, Italy
| | - Antonia Giacco
- Department of Sciences and Technologies, University of Sannio, Benevento, Italy
| | - Federica Cioffi
- Department of Sciences and Technologies, University of Sannio, Benevento, Italy
| | - Arianna Mazzoli
- Department of Biology, University of Naples Federico II, Naples, Italy
| | - Nunzia Magnacca
- Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, University of Campania "L. Vanvitelli", Caserta, Italy
| | - Susanna Iossa
- Department of Biology, University of Naples Federico II, Naples, Italy
| | - Fernando Goglia
- Department of Sciences and Technologies, University of Sannio, Benevento, Italy
| | - Rosalba Senese
- Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, University of Campania "L. Vanvitelli", Caserta, Italy
| | - Antonia Lanni
- Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, University of Campania "L. Vanvitelli", Caserta, Italy
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14
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O'Connor G, Edel L, Raquq S, Bowerman M, Szmurlo A, Simpson Z, Hardy I, Fewtrell M, Baranello G. Open-labelled study to monitor the effect of an amino acid formula on symptom management in children with spinal muscular atrophy type I: The SMAAF pilot study. Nutr Clin Pract 2022. [PMID: 36504203 DOI: 10.1002/ncp.10940] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/28/2022] [Revised: 11/02/2022] [Accepted: 11/05/2022] [Indexed: 12/14/2022] Open
Abstract
BACKGROUND An increasing number of families with children who have spinal muscular atrophy (SMA) are incorporating a special amino acid diet into their child's feeding regimens. Characteristics of the diet include high-carbohydrate and low-fat content with added probiotics. However, because of insufficient evidenced-based research, clinicians are unable to prescribe or endorse this diet. Our aim was to assess the tolerability of an adapted version of the traditional amino acid diet in children with SMA type I. METHODS Children with SMA type I were recruited if they were enterally fed and experienced at least one gastrointestinal symptom (reflux, vomiting, constipation, and/or diarrhea). Children were transitioned to an amino acid formula (Neocate Syneo-Nutricia) for 8 weeks. Feeding tolerance was measured weekly by telephone consultation to monitor reflux, vomiting, stool consistency, and frequency. RESULTS Fourteen children were recruited, the mean age was 4.1 years (±1.2 SD), and 64% of participants were female. The mean resting energy expenditure determined by indirect calorimetry was 51.5 kcal/kg (±7 SD). The most common gastrointestinal complaint before switching to the amino acid formula was constipation, which was reported in 12 of 14 (85%) patients, of which 10 of the 12 (83%) children required daily stool softeners/laxatives to help regulate bowel function. After 8 weeks on the amino acid formula, 10 out of 12 (83%) children stopped or reduced constipation medication. CONCLUSION Children with SMA type I who display gastrointestinal symptoms such as constipation and reflux may benefit from an amino acid formula that is fortified with probiotics.
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Affiliation(s)
- Graeme O'Connor
- Dietetic Department, Great Ormond Street Hospital Foundation Trust, London, UK
| | - Lisa Edel
- Physiotherapy Department, Great Ormond Street Hospital Foundation Trust, London, UK
| | - Sarah Raquq
- Developmental Neuroscience Research & Teaching Department, Dubowitz Neuromuscular Centre, UCL Great Ormond Street Institute of Child Health, NHS Foundation Trust, London, UK
| | - Melissa Bowerman
- School of Medicine, Keele University, Keele, Staffordshire, UK.,Wolfson Centre for Inherited Neuromuscular Disease, Oswestry, Shropshire, UK
| | - Agnieszka Szmurlo
- Dietetic Department, Great Ormond Street Hospital Foundation Trust, London, UK
| | - Zoe Simpson
- Dietetic Department, Great Ormond Street Hospital Foundation Trust, London, UK
| | - Isobel Hardy
- Dietetic Department, Great Ormond Street Hospital Foundation Trust, London, UK
| | - Mary Fewtrell
- Population, Policy & Practice Department, UCL Great Ormond Street Institute of Child Health, Faculty of Population Health Sciences, London, UK
| | - Giovanni Baranello
- Developmental Neuroscience Research & Teaching Department, Dubowitz Neuromuscular Centre, UCL Great Ormond Street Institute of Child Health, NHS Foundation Trust, London, UK
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15
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Freedman LS, Kipnis V, Midthune D, Commins J, Barrett B, Sagi-Kiss V, Palma-Duran SA, Johnston CS, O'Brien DM, Tasevska N. Establishing 24-Hour Urinary Sucrose Plus Fructose as a Predictive Biomarker for Total Sugars Intake. Cancer Epidemiol Biomarkers Prev 2022; 31:1227-1232. [PMID: 35314857 DOI: 10.1158/1055-9965.epi-21-1293] [Citation(s) in RCA: 6] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/10/2021] [Revised: 12/21/2021] [Accepted: 03/02/2022] [Indexed: 02/06/2023] Open
Abstract
BACKGROUND Twenty-four-hour urinary sucrose and fructose (24uSF) has been studied as a biomarker of total sugars intake in two feeding studies conducted in the United Kingdom (UK) and Arizona (AZ). We compare the biomarker performance in these populations, testing whether it meets the criteria for a predictive biomarker. METHODS The UK and AZ feeding studies included 13 and 98 participants, respectively, aged 18 to 70 years, consuming their usual diet under controlled conditions. Linear mixed models relating 24uSF to total sugars and personal characteristics were developed in each study and compared. The AZ calibrated biomarker equation was applied to generate biomarker-estimated total sugars intake in UK participants. Stability of the model across AZ study subpopulations was also examined. RESULTS Model coefficients were similar between the two studies [e.g., log(total sugars): UK 0.99, AZ 1.03, P = 0.67], as was the ratio of calibrated biomarker person-specific bias to between-person variance (UK 0.32, AZ 0.25, P = 0.68). The AZ equation estimated UK log(total sugar intakes) with mean squared prediction error of 0.27, similar to the AZ study estimate (0.28). Within the AZ study, the regression coefficients of log(total sugars) were similar across age, gender, and body mass index subpopulations. CONCLUSIONS Similar model coefficients in the two studies and good prediction of UK sugar intakes by the AZ equation suggest that 24uSF meets the criteria for a predictive biomarker. Testing the biomarker performance in other populations is advisable. IMPACT Applications of the 24uSF biomarker will enable improved assessment of the role of sugars intake in risk of chronic disease, including cancer. See related commentary by Prentice, p. 1151.
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Affiliation(s)
- Laurence S Freedman
- Gertner Institute for Epidemiology and Health Policy Research, Sheba Medical Center, Tel Hashomer, Israel
| | - Victor Kipnis
- Division of Cancer Prevention, NCI, Bethesda, Maryland
| | | | - John Commins
- Information Management Services, Inc., Rockville, Maryland
| | - Brian Barrett
- Information Management Services, Inc., Rockville, Maryland
| | - Virag Sagi-Kiss
- College of Health Solutions, Arizona State University, Phoenix, Arizona
| | | | - Carol S Johnston
- College of Health Solutions, Arizona State University, Phoenix, Arizona
| | - Diane M O'Brien
- Institute of Arctic Biology, University of Alaska Fairbanks, Fairbanks, Alaska
| | - Natasha Tasevska
- College of Health Solutions, Arizona State University, Phoenix, Arizona
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16
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Buziau AM, Eussen SJPM, Kooi ME, van der Kallen CJH, van Dongen MCJM, Schaper NC, Henry RMA, Schram MT, Dagnelie PC, van Greevenbroek MMJ, Wesselius A, Bekers O, Meex SJR, Schalkwijk CG, Stehouwer CDA, Brouwers MCGJ. Fructose Intake From Fruit Juice and Sugar-Sweetened Beverages Is Associated With Higher Intrahepatic Lipid Content: The Maastricht Study. Diabetes Care 2022; 45:1116-1123. [PMID: 35158374 DOI: 10.2337/dc21-2123] [Citation(s) in RCA: 9] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/12/2021] [Accepted: 01/01/2022] [Indexed: 02/03/2023]
Abstract
OBJECTIVE Epidemiological evidence regarding the relationship between fructose intake and intrahepatic lipid (IHL) content is inconclusive. We, therefore, assessed the relationship between different sources of fructose and IHL at the population level. RESEARCH DESIGN AND METHODS We used cross-sectional data from The Maastricht Study, a population-based cohort study (n = 3,981; mean ± SD age: 60 ± 9 years; 50% women). We assessed the relationship between fructose intake (assessed with a food-frequency questionnaire)-total and derived from fruit, fruit juice, and sugar-sweetened beverages (SSB)-and IHL (quantified with 3T Dixon MRI) with adjustment for age, sex, type 2 diabetes, education, smoking status, physical activity, and intakes of total energy, alcohol, saturated fat, protein, vitamin E, and dietary fiber. RESULTS Energy-adjusted total fructose intake and energy-adjusted fructose from fruit were not associated with IHL in the fully adjusted models (P = 0.647 and P = 0.767). In contrast, energy-adjusted intake of fructose from fruit juice and SSB was associated with higher IHL in the fully adjusted models (P = 0.019 and P = 0.009). Individuals in the highest tertile of energy-adjusted intake of fructose from fruit juice and SSB had a 1.04-fold (95% CI 0.99; 1.11) and 1.09-fold (95% CI 1.03; 1.16) higher IHL, respectively, in comparison with the lowest tertile in the fully adjusted models. Finally, the association for fructose from fruit juice was stronger in individuals with type 2 diabetes (P for interaction = 0.071). CONCLUSIONS Fructose from fruit juice and SSB is independently associated with higher IHL. These cross-sectional findings contribute to current knowledge in support of measures to reduce the intake of fructose-containing beverages as a means to prevent nonalcoholic fatty liver disease at the population level.
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Affiliation(s)
- Amée M Buziau
- Division of Endocrinology and Metabolic Disease, Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands.,School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Laboratory for Metabolism and Vascular Medicine, Division of General Internal Medicine, Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands
| | - Simone J P M Eussen
- School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Department of Epidemiology, Maastricht University, Maastricht, the Netherlands.,Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht, the Netherlands
| | - M Eline Kooi
- School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Department of Radiology and Nuclear Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands
| | - Carla J H van der Kallen
- School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands
| | - Martien C J M van Dongen
- Department of Epidemiology, Maastricht University, Maastricht, the Netherlands.,Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht, the Netherlands
| | - Nicolaas C Schaper
- Division of Endocrinology and Metabolic Disease, Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands.,School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht, the Netherlands
| | - Ronald M A Henry
- School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands.,Heart & Vascular Centre, Maastricht University Medical Center+, Maastricht, the Netherlands
| | - Miranda T Schram
- School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands.,Heart & Vascular Centre, Maastricht University Medical Center+, Maastricht, the Netherlands
| | - Pieter C Dagnelie
- School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands
| | - Marleen M J van Greevenbroek
- School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Laboratory for Metabolism and Vascular Medicine, Division of General Internal Medicine, Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands
| | - Anke Wesselius
- School for Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, Maastricht, the Netherlands.,Department of Complex Genetics and Epidemiology, Maastricht University, Maastricht, the Netherlands
| | - Otto Bekers
- School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Central Diagnostic Laboratory, Department of Clinical Chemistry, Maastricht University Medical Center+, Maastricht, the Netherlands
| | - Steven J R Meex
- School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Central Diagnostic Laboratory, Department of Clinical Chemistry, Maastricht University Medical Center+, Maastricht, the Netherlands
| | - Casper G Schalkwijk
- School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Laboratory for Metabolism and Vascular Medicine, Division of General Internal Medicine, Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands
| | - Coen D A Stehouwer
- School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands.,Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands
| | - Martijn C G J Brouwers
- Division of Endocrinology and Metabolic Disease, Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, the Netherlands.,School for Cardiovascular Diseases (CARIM), Maastricht University, Maastricht, the Netherlands
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17
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Milton-Laskibar I, Marcos-Zambrano LJ, Gómez-Zorita S, Carrillo de Santa Pau E, Fernández-Quintela A, Martínez JA, Portillo MP. Involvement of microbiota and short-chain fatty acids on non-alcoholic steatohepatitis when induced by feeding a hypercaloric diet rich in saturated fat and fructose. GUT MICROBIOME (CAMBRIDGE, ENGLAND) 2022; 3:e5. [PMID: 39295781 PMCID: PMC11406367 DOI: 10.1017/gmb.2022.2] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Subscribe] [Scholar Register] [Received: 06/16/2021] [Revised: 03/08/2022] [Accepted: 04/05/2022] [Indexed: 09/21/2024]
Abstract
Consumption of high-energy-yielding diets, rich in fructose and lipids, is a factor contributing to the current increase in non-alcoholic fatty liver disease prevalence. Gut microbiota composition and short-chain fatty acids (SCFAs) production alterations derived from unhealthy diets are considered putative underlying mechanisms. This study aimed to determine relationships between changes in gut microbiota composition and SCFA levels by comparing rats featuring diet-induced steatohepatitis with control counterparts fed a standard diet. A high-fat high-fructose (HFHF) feeding induced higher body, liver and mesenteric adipose tissue weights, increased liver triglyceride content and serum transaminase, glucose, non-HDL-c and MCP-1 levels. Greater liver malondialdehyde levels and glutathione peroxidase activity were also observed after feeding the hypercaloric diet. Regarding gut microbiota composition, a lowered diversity and increased abundances of bacteria from the Clostridium sensu stricto 1, Blautia, Eubacterium coprostanoligenes group, Flavonifractor, and UBA1819 genera were found in rats featuring diet-induced steatohepatitis, as well as higher isobutyric, valeric and isovaleric acids concentrations. These results suggest that hepatic alterations produced by a hypercaloric HFHF diet may be related to changes in overall gut microbiota composition and abundance of specific bacteria. The shift in SCFA levels produced by this unbalanced diet cannot be discarded as potential mediators of the reported hepatic and metabolic alterations.
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Affiliation(s)
- Iñaki Milton-Laskibar
- Precision Nutrition and Cardiometabolic Health Program, IMDEA Food Institute (Madrid Institute for Advanced Studies), Campus of International Excellence (CEI) UAM+CSIC, Spanish National Research Council, Madrid, Spain
- CIBEROBN Physiopathology of Obesity and Nutrition, Institute of Health Carlos III (ISCIII), Madrid, Spain
| | - Laura Judith Marcos-Zambrano
- Computational Biology Group, Precision Nutrition and Cancer Research Program, IMDEA Food Institute, Madrid, Spain
| | - Saioa Gómez-Zorita
- CIBEROBN Physiopathology of Obesity and Nutrition, Institute of Health Carlos III (ISCIII), Madrid, Spain
- Nutrition and Obesity group, Department of Pharmacy and Food Science, Faculty of Pharmacy, Lucio Lascaray Research Center, University of the Basque Country (UPV/EHU), Vitoria-Gasteiz, Spain
- BIOARABA Health Research Institute, Vitoria-Gasteiz, Spain
| | | | - Alfredo Fernández-Quintela
- CIBEROBN Physiopathology of Obesity and Nutrition, Institute of Health Carlos III (ISCIII), Madrid, Spain
- Nutrition and Obesity group, Department of Pharmacy and Food Science, Faculty of Pharmacy, Lucio Lascaray Research Center, University of the Basque Country (UPV/EHU), Vitoria-Gasteiz, Spain
- BIOARABA Health Research Institute, Vitoria-Gasteiz, Spain
| | - Jose Alfredo Martínez
- CIBEROBN Physiopathology of Obesity and Nutrition, Institute of Health Carlos III (ISCIII), Madrid, Spain
| | - María Puy Portillo
- CIBEROBN Physiopathology of Obesity and Nutrition, Institute of Health Carlos III (ISCIII), Madrid, Spain
- Nutrition and Obesity group, Department of Pharmacy and Food Science, Faculty of Pharmacy, Lucio Lascaray Research Center, University of the Basque Country (UPV/EHU), Vitoria-Gasteiz, Spain
- BIOARABA Health Research Institute, Vitoria-Gasteiz, Spain
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18
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Abstract
Nonalcoholic fatty liver disease (NAFLD) can develop in lean individuals. Despite a better metabolic profile, the risk of disease progression to hepatic inflammation, fibrosis, and decompensated cirrhosis in the lean is similar to that in obesity-related NAFLD and lean individuals may experience more severe hepatic consequences and higher mortality relative to those with a higher body mass index (BMI). In the absence of early symptoms and abnormal laboratory findings, lean individuals are not likely to be screened for NAFLD or related comorbidities; however, given the progressive nature of the disease and the increased risk of morbidity and mortality, a clearer understanding of the natural history of NAFLD in lean individuals, as well as efforts to raise awareness of the potential health risks of NAFLD in lean individuals, are warranted. In this review, we summarize available data on NAFLD prevalence, clinical characteristics, outcomes, and mortality in lean individuals and discuss factors that may contribute to the development of NAFLD in this population, including links between dietary and genetic factors, menopausal status, and ethnicity. We also highlight the need for greater representation of lean individuals in NAFLD-related clinical trials, as well as more studies to better characterize lean NAFLD, develop improved screening algorithms, and determine specific treatment strategies based on underlying etiology.
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Affiliation(s)
- Johanna K. DiStefano
- Diabetes and Fibrotic Disease Research Unit, Translational Genomics Research Institute, Phoenix, USA
| | - Glenn S. Gerhard
- Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA 19140 USA
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19
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Jeyakumar SM, Vajreswari A. Stearoyl-CoA desaturase 1: A potential target for non-alcoholic fatty liver disease?-perspective on emerging experimental evidence. World J Hepatol 2022; 14:168-179. [PMID: 35126846 PMCID: PMC8790397 DOI: 10.4254/wjh.v14.i1.168] [Citation(s) in RCA: 26] [Impact Index Per Article: 8.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/03/2021] [Revised: 06/18/2021] [Accepted: 12/10/2021] [Indexed: 02/06/2023] Open
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a progressive disease and one of the leading causes of death. An unnamed disease has become a global epidemic disease of public health concern. This spectrum of diseases manifests itself with initial accumulation of excessive triglycerides (due to de novo lipogenesis) in the hepatocytes, leading to simple steatosis. Although its aetiology is multi-factorial, lifestyle changes (diet and physical activity) are considered to be the key thriving factors. In this context, high fructose consumption is associated with an increased risk for developing NAFLD in humans, while high-fructose feeding to experimental animals results in hepatic steatosis and non-alcoholic steatohepatitis, by increasing hepatic lipogenesis. Among several lipogenic genes, the endoplasmic reticulum-bound stearoyl-CoA desaturase 1 (SCD1) is the key determinant of triglycerides biosynthesis pathway, by providing monounsaturated fatty acids, through the incorporation of a double bond at the delta-9 position of saturated fatty acids, specifically, palmitic (C16:0) and stearic (C18:0) acids, yielding palmitoleic (C16:1) and oleic (C18:1) acids, respectively. Various experimental studies involving SCD1 gene knockout and diet-induced rodent models have demonstrated that SCD1 plays a key role in the development of NAFLD, by modulating hepatic lipogenesis and thus triglyceride accumulation in the liver. Several pharmacological and dietary intervention studies have shown the benefits of inhibiting hepatic SCD1 in the pathogenesis of NAFLD. In this review, we give an overview of SCD1 in NAFLD, based on the current experimental evidence and the translational applicability of SCD1 inhibition in human NAFLD conditions, besides discussing the limitations and way-forward.
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Affiliation(s)
- Shanmugam Murugaiha Jeyakumar
- Division of Lipid Biochemistry, National Institute of Nutrition, Hyderabad 500007, Telangana, India
- Department of Clinical Pharmacology, National Institute for Research in Tuberculosis, Chennai 600031, Tamil Nadu, India
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20
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Moreira-Silva H, Ferreira S, Almeida M, Gonçalves I, Cipriano MA, Vizcaíno JR, Santos-Silva E, Gomes-Martins E. Case report: NAFLD and maple syrup urine disease: Is there an interplay between branched-chain amino acids and fructose consumption? Front Pediatr 2022; 10:933081. [PMID: 36299693 PMCID: PMC9589422 DOI: 10.3389/fped.2022.933081] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/30/2022] [Accepted: 09/02/2022] [Indexed: 12/03/2022] Open
Abstract
BACKGROUND The worldwide increase in pediatric overweight and obesity, in parallel with the global increase in the consumption of sucrose and fructose, is associated with non-alcoholic fatty liver disease (NAFLD). Elevated branched-chain amino acids (BCAAs) are a metabolic feature related to obesity and an early risk factor for insulin resistance and NAFLD. However, few studies have assessed metabolic risk factors and nutritional status in maple syrup urine disease (MSUD) patients under restricted BCAA and high carbohydrate diets. METHODS AND RESULTS Herein, we present a pilot report of a 17-year-old boy with classic MSUD with poor diet compliance and high fructose consumption, mainly during early adolescence. At that time, he was overweight and developed features of metabolic syndrome, including persistently elevated liver enzymes and hepatic steatosis. He underwent liver transplantation at the age of 13 years to prevent the risk of progressive cognitive impairment. Two months later, NAFLD relapsed in the graft, despite a better BCAA balance and weight loss. Nevertheless, 6 months after dietary restriction of fructose consumption, NAFLD had sustainably improved. CONCLUSION Childhood overweight and fructose overconsumption are wellestablished driving forces in the development of pediatric NAFLD. However, their role in the early onset and progression of NAFLD in the allograft remains to be established. Furthermore, it is not known whether the dysmetabolic state associated with elevated BCAAs may be contributory. Further studies are required with a cohort of MSUD subjects to validate our findings and to ascertain the possible interaction between a BCAA imbalance and dietary intake in the development of NAFLD.
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Affiliation(s)
- Helena Moreira-Silva
- Pediatric Gastroenterology Unit, Centro Materno Infantil do Norte, Centro Hospitalar Universitário do Porto, Porto, Portugal
| | - Sandra Ferreira
- Hepatology and Pediatric Liver Transplantation Unit, Hospital Pediátrico de Coimbra, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal
| | - Manuela Almeida
- Pediatric Metabolic Diseases Unit, Centro de Referência de Doenças Hereditárias do Metabolismo, Centro Hospitalar Universitário do Porto, Porto, Portugal
| | - Isabel Gonçalves
- Hepatology and Pediatric Liver Transplantation Unit, Hospital Pediátrico de Coimbra, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal
| | | | - J R Vizcaíno
- Anatomic Pathology Service, Pathology Department, Centro Hospitalar Universitário do Porto, Porto, Portugal
| | - Ermelinda Santos-Silva
- Pediatric Gastroenterology Unit, Centro Materno Infantil do Norte, Centro Hospitalar Universitário do Porto, Porto, Portugal
| | - Esmeralda Gomes-Martins
- Pediatric Metabolic Diseases Unit, Centro de Referência de Doenças Hereditárias do Metabolismo, Centro Hospitalar Universitário do Porto, Porto, Portugal
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21
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Zhu B, Chan SL, Li J, Li K, Wu H, Cui K, Chen H. Non-alcoholic Steatohepatitis Pathogenesis, Diagnosis, and Treatment. Front Cardiovasc Med 2021; 8:742382. [PMID: 34557535 PMCID: PMC8452937 DOI: 10.3389/fcvm.2021.742382] [Citation(s) in RCA: 19] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/16/2021] [Accepted: 08/13/2021] [Indexed: 12/12/2022] Open
Abstract
There has been a rise in the prevalence of non-alcohol fatty liver disease (NAFLD) due to the popularity of western diets and sedentary lifestyles. One quarter of NAFLD patients is diagnosed with non-alcoholic steatohepatitis (NASH), with histological evidence not only of fat accumulation in hepatocytes but also of liver cell injury and death due to long-term inflammation. Severe NASH patients have increased risks of cirrhosis and liver cancer. In this review, we discuss the pathogenesis and current methods of diagnosis for NASH, and current status of drug development for this life-threatening liver disease.
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Affiliation(s)
| | | | | | | | | | | | - Hong Chen
- Department of Surgery, Vascular Biology Program, Harvard Medical School, Boston Children's Hospital, Boston, MA, United States
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22
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Gut Microbiota Induced by Pterostilbene and Resveratrol in High-Fat-High-Fructose Fed Rats: Putative Role in Steatohepatitis Onset. Nutrients 2021; 13:nu13051738. [PMID: 34065444 PMCID: PMC8160898 DOI: 10.3390/nu13051738] [Citation(s) in RCA: 9] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/21/2021] [Revised: 05/14/2021] [Accepted: 05/18/2021] [Indexed: 02/06/2023] Open
Abstract
Resveratrol and its 2-methoxy derivative pterostilbene are two phenolic compounds that occur in foodstuffs and feature hepato-protective effects. This study is devoted to analysing and comparing the metabolic effects of pterostilbene and resveratrol on gut microbiota composition in rats displaying NAFLD induced by a diet rich in saturated fat and fructose. The associations among changes induced by both phenolic compounds in liver status and those induced in gut microbiota composition were also analysed. For this purpose, fifty Wistar rats were distributed in five experimental groups: a group of animals fed a standard diet (CC group) and four additional groups fed a high-fat high-fructose diet alone (HFHF group) or supplemented with 15 or 30 mg/kg bw/d of pterostilbene (PT15 and PT30 groups, respectively) or 30 mg/kg bw/d of resveratrol (RSV30 group). The dramatic changes induced by high-fat high-fructose feeding in the gut microbiota were poorly ameliorated by pterostilbene or resveratrol. These results suggest that the specific changes in microbiota composition induced by pterostilbene (increased abundances of Akkermansia and Erysipelatoclostridium, and lowered abundance of Clostridum sensu stricto 1) may not entirely explain the putative preventive effects on steatohepatitis.
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23
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Ilias I, Goulas S, Zabuliene L. Polycystic ovary syndrome: Pathways and mechanisms for possible increased susceptibility to COVID-19. World J Clin Cases 2021; 9:2711-2720. [PMID: 33969054 PMCID: PMC8058679 DOI: 10.12998/wjcc.v9.i12.2711] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/19/2020] [Revised: 01/16/2021] [Accepted: 03/18/2021] [Indexed: 02/06/2023] Open
Abstract
In 75% of women with polycystic ovary syndrome (PCOS), insulin action is impaired. In obesity, visceral adipose tissue becomes dysfunctional: Chronic inflammation is favored over storage, contributing to the development of metabolic complications. PCOS, metabolic syndrome (MetSy) and non-alcoholic fatty liver disease (NAFLD) apparently share common pathogenic factors; these include abdominal adiposity, excess body weight and insulin resistance. Alterations in the gut microbiome have been noted in women with PCOS compared to controls; these may lead to deterioration of the intestinal barrier, increased gut mucosal permeability and immune system activation, hyperinsulinemia and glucose intolerance, which hamper normal ovarian function and follicular development (all being hallmarks of PCOS). It has been proposed that PCOS may entail higher susceptibility to coronavirus disease 2019 (COVID-19) via its associated comorbidities (NAFLD, obesity, MetSy and alterations in the gut microbiome). Studies have found an association between acute respiratory distress syndrome (seen in severe cases of COVID-19) and the intestinal microbiome. Furthermore, apparently, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can gain entry to the gastrointestinal tract via locally-expressed angiotensin converting enzyme type 2 receptors. Excess body weight is associated with more severe COVID-19 and increased mortality. Although robust links between SARS-CoV-2 infection and PCOS/NAFLD/gut microbiome/metabolic consequences are yet to be confirmed, it seems that strategies for adapting the intestinal microbiome could help reduce the severity of COVID-19 in women with PCOS with or without NAFLD, MetSy or obesity.
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Affiliation(s)
- Ioannis Ilias
- Department of Endocrinology, Elena Venizelou Hospital, Athens GR-11521, Greece
| | - Spyridon Goulas
- Department of Gastroenterology Unit, Elena Venizelou Hospital, Athens GR-11521, Greece
| | - Lina Zabuliene
- Institute of Clinical Medicine, Faculty of Medicine, Vilnius University, Vilnius LT-03101, Lithuania
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24
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Lazebnik LB, Golovanova EV, Turkina SV, Raikhelson KL, Okovityy SV, Drapkina OM, Maev IV, Martynov AI, Roitberg GE, Khlynova OV, Abdulganieva DI, Alekseenko SA, Ardatskaya MD, Bakulin IG, Bakulina NV, Bueverov AO, Vinitskaya EV, Volynets GV, Eremina EY, Grinevich VB, Dolgushina AI, Kazyulin AN, Kashkina EI, Kozlova IV, Konev YV, Korochanskaya NV, Kravchuk YA, Li ED, Loranskaya ID, Makhov VM, Mekhtiev SN, Novikova VP, Ostroumova OD, Pavlov CS, Radchenko VG, Samsonov AA, Sarsenbaeva AS, Sayfutdinov RG, Seliverstov PV, Sitkin SI, Stefanyuk OV, Tarasova LV, Tkachenko EI, Uspensky YP, Fominykh YA, Khavkin AI, Tsyganova YV, Sharhun OO. Non-alcoholic fatty liver disease in adults: clinic, diagnostics, treatment. Guidelines for therapists, third version. EXPERIMENTAL AND CLINICAL GASTROENTEROLOGY 2021; 1:4-52. [DOI: 10.31146/1682-8658-ecg-185-1-4-52] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 09/26/2023]
Affiliation(s)
- L. B. Lazebnik
- Federal State Budgetary Educational Institution of Higher Education “A. I. Yevdokimov Moscow State University of Medicine and Dentistry” of the Ministry of Healthcare of the Russion Federation
| | - E. V. Golovanova
- Federal State Budgetary Educational Institution of Higher Education “A. I. Yevdokimov Moscow State University of Medicine and Dentistry” of the Ministry of Healthcare of the Russion Federation
| | - S. V. Turkina
- State-funded Educational Establishment of Higher Professional Education «Volgograd State Medical University of the Ministry of Public Health of the Russian Federation»
| | | | - S. V. Okovityy
- Saint Petersburg State Chemical Pharmaceutical University (SPCPA)
| | - O. M. Drapkina
- National Medical Research Center for Therapy and Preventive Medicine of the Russian Ministry of Health
| | - I. V. Maev
- Federal State Budgetary Educational Institution of Higher Education “A. I. Yevdokimov Moscow State University of Medicine and Dentistry” of the Ministry of Healthcare of the Russion Federation
| | - A. I. Martynov
- Federal State Budgetary Educational Institution of Higher Education “A. I. Yevdokimov Moscow State University of Medicine and Dentistry” of the Ministry of Healthcare of the Russion Federation
| | - G. E. Roitberg
- Pirogov Russian National Research Medical University; JSC «Medicine»
| | - O. V. Khlynova
- Perm State Medical University named after academician E. A. Vagner Ministry of Health care of Russia
| | | | | | - M. D. Ardatskaya
- Federal State Budgetary Institution “Central Clinical Hospital”, of the Russian Federation Presidential Administration
| | - I. G. Bakulin
- North- Western state medical University named after I. I. Mechnikov, Ministry of health of the Russian Federation
| | - N. V. Bakulina
- North- Western state medical University named after I. I. Mechnikov, Ministry of health of the Russian Federation
| | - A. O. Bueverov
- Moscow regional research and clinical Institute of M. F. Vladimirsky
| | | | | | | | | | | | - A. N. Kazyulin
- Federal State Budgetary Educational Institution of Higher Education “A. I. Yevdokimov Moscow State University of Medicine and Dentistry” of the Ministry of Healthcare of the Russion Federation
| | | | - I. V. Kozlova
- Saratov State Medical University n. a. V. I. Razumovsky
| | - Yu. V. Konev
- Federal State Budgetary Educational Institution of Higher Education “A. I. Yevdokimov Moscow State University of Medicine and Dentistry” of the Ministry of Healthcare of the Russion Federation
| | - N. V. Korochanskaya
- Federal State Budgetary Educational Institution of Higher Education Kuban State Medical University Health Ministry of Russian Federation
| | | | - E. D. Li
- Multifunctional medical center of the Bank of Russia
| | - I. D. Loranskaya
- Federal State Budgetary Educational Institution of Further Professional Education “Russian Medical Academy of Continuous Professional Education” of the Ministry of Healthcare of the Russian Federation
| | - V. M. Makhov
- I. M. Sechenov First Moscow Medical State University
| | - S. N. Mekhtiev
- Institute of Professional Retraining of the International Medical Center “SOGAZ”
| | | | - O. D. Ostroumova
- Federal State Budgetary Educational Institution of Further Professional Education “Russian Medical Academy of Continuous Professional Education” of the Ministry of Healthcare of the Russian Federation
| | - Ch. S. Pavlov
- I. M. Sechenov First Moscow Medical State University
| | | | - A. A. Samsonov
- Federal State Budgetary Educational Institution of Higher Education “A. I. Yevdokimov Moscow State University of Medicine and Dentistry” of the Ministry of Healthcare of the Russion Federation
| | | | - R. G. Sayfutdinov
- Kazan State Medical Academy — Branch Campus of the Federal State Budgetary Educational Institution of Further Professional Education “Russian Medical Academy of Continuous Professional Education” of the Ministry of Healthcare of the Russian Federation, central scientifi c research laboratory
| | - P. V. Seliverstov
- North-Western state medical University named after I. I. Mechnikov, Ministry of health of the Russian Federation
| | - S. I. Sitkin
- North-Western state medical University named after I. I. Mechnikov, Ministry of health of the Russian Federation
| | - O. V. Stefanyuk
- Federal State Budgetary Educational Institution of Higher Education “A. I. Yevdokimov Moscow State University of Medicine and Dentistry” of the Ministry of Healthcare of the Russion Federation; National Medical Research Center for Therapy and Preventive Medicine of the Russian Ministry of Health
| | | | | | | | | | - A. I. Khavkin
- Pirogov Russian National Research Medical University
| | | | - O. O. Sharhun
- Pirogov Russian National Research Medical University
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