This study evaluated the effects of maximal and submaximal exercise training on serum levels of Asprosin, insulin resistance, and body composition in overweight and obese women.

30 overweight/obese women voluntarily participated in the study and were then randomly divided into control, submaximal, and maximal groups. A treadmill high-intensity exercise protocol was applied to MG non-consecutive three days a week for 8 weeks, in four 4-min intervals with an intensity of 70 to 95% of maximum heart rate (HRmax) with 3-min active recovery intervals. SMG performed a moderate-intensity exercise protocol of approximately 25 to 35 min at the treadmill at 50-70% of HRmax non-consecutive days three days per week for 8 weeks. The CG continued their daily routine activities. Anthropometric and body composition measurements such as body weight, height, BMI, and waist-hip ratio (WHR) were performed before and after the 8-week training period. Fasting blood glucose (FGB), insulin, insulin resistance (HOMA-IR), and serum asprosin levels were also measured.

Post-training, there were significant main effects of time and a group-by-time interaction for all body composition and performance variables (p < 0.001). Post hoc analysis revealed that body mass, BMI, WHR, FBG, insulin, HOMA-IR, and serum asprosin were significantly reduced after 8 8-week training program.

The present study showed that maximal and submaximal exercise protocols effectively improved body composition, insulin sensitivity, resistance, and reduced asprosin level. It has been concluded that these effects are more pronounced, especially after maximal exercise protocols.

Energy-restricted (ER) diets promote weight loss and improve body composition and glycaemic control. Nut consumption also improves these parameters. However, less is known about the combined benefit of these two strategies. This scoping review implemented a systematic search of Medline, Embase and Scopus to identify randomised controlled trials evaluating the effect of ER diets with or without nuts on body mass, body composition and glycaemic control in adults. After reviewing titles and abstracts, twenty-nine full-text articles were screened, resulting in seven studies reported in eight papers that met the inclusion criteria. Energy restriction was achieved by prescribing a set energy target or reducing intake by 1000-4200 kJ from daily energy requirements. Interventions ranged from 4 to 52 weeks in duration and contained 42-84 g/d of almonds, peanuts, pistachios or walnuts. While all studies reported that energy restriction resulted in significant weight loss, the addition of nuts to ER diets demonstrated significantly greater weight loss in only approximately half of the included studies (4/7 studies). There was limited evidence to support additional benefits from nuts for body composition measures or glycaemic control. Although improvements in weight loss and glycaemia were not consistent when nuts were included in ER diets, no study revealed an adverse effect of nut consumption on health outcomes. Future studies could explore the effect of consuming different types and amounts of nuts, combined with various levels of energy restriction on weight, body composition and glycaemic control.

Systemic inflammation and oxidative stress are known to exacerbate airway inflammation in asthma. Obesity contributes to this pathophysiology.

To determine the relationship between obesity, disease severity, disease control, and oxidative stress in asthma with multiple oxidative stress markers.

The study included 65 obese-asthma (OA), 25 non-obese asthma (A), and 30 healthy non-obese controls (C). Skin prick tests, lung functions, and 8-isoprostane levels in urine samples were measured. Exhaled breath condensate (EBC) was tested for 8-isoprostane, glutathione peroxidase, and malondialdehyde (MDA). Serum samples were taken for adiponectin and leptin.

OA leptin levels were higher than those of the A and C groups (p < 0.001). Glutathione peroxidase levels in EBC were found to be different between groups (p = 0.016), while there was no difference in two-group comparisons. MDA levels were significant (p < 0.001) between groups, with the A group's lower levels contributing to this significance. 8-isoprostane levels were greater in the OA group than in other groups (p = 0.005). This significance came from the difference between the OA and A groups (p = 0.005). Urine 8-isoprostane levels were different between groups (p = 0.001), and the OA group had lower levels than the A group (p = 0.003). In EBC, there were positive correlations between BMI and MDA (p < 0.001, r = 0.484) and 8-isoprostane (p < 0.001, r = 0.471). Patients with uncontrolled/partially-controlled asthma had greater levels of MDA and 8-isoprostane than those with well-controlled asthma (p = 0.036 and p = 0.011).

Elevated levels of MDAand 8-isoprostane in EBC in obese asthma support that obesity increases oxidative stress markers. This relationship indicate that antioxidant therapies may be beneficial in OA patients. EBC is a reliable and noninvasive technique for measuring oxidative inflammation.

To explore the relationships between second-trimester anthropometric obesity indicators and cesarean section (CS).

A retrospective study was conducted at West China Second University Hospital, utilizing electronic health records from 15,304 pregnant women who received routine prenatal care and delivered between January 2021 and June 2022. Second-trimester anthropometric indicators, including body roundness index (BRI), body mass index (BMI), body fat percentage (BFP), and waist circumference (WC), were measured using bioelectrical impedance analysis (BIA). Logistic regression models were employed to assess the associations between these indicators and CS risk, with additional subgroup analyses based on maternal age and fetal sex.

The mean maternal age was 30.13 years. After adjusting for covariates, BRI (OR 1.22, 95%CI 1.15-1.30), BMI (OR 1.07, 95%CI 1.05-1.08), BFP (OR 1.03, 95%CI 1.02-1.04), and WC (OR 1.02, 95%CI 1.01-1.03) were all significantly associated with CS. Stratified analyses based on maternal age and fetal sex further confirmed these independent associations.

Second-trimester BRI, BMI, BFP, and WC were all significantly associated with CS risk, with BRI potentially demonstrating the strongest independent correlation. An integrated approach incorporating BMI and WC is recommended for CS risk, particularly in time-sensitive or resource-limited settings. The effect of anthropometric changes during pregnancy on CS may be explored in the future.

Periodontal diseases, including gingivitis and periodontitis, are chronic inflammatory conditions that compromise the supporting structures of the teeth, often leading to tooth loss and contributing to systemic comorbidities. Increasing evidence underscores the critical role of modifiable lifestyle factors, particularly diet and physical activity, in influencing periodontal health. This narrative review critically evaluates the current body of literature regarding the impact of dietary constituents and physical activity on the periodontium, with a focus on the molecular mechanisms, key biomarkers, and clinical implications. It aims to provide a deeper understanding of the complex interactions between nutrition, exercise, and periodontal health with potential implications for clinical management and preventive strategies.

Introduction: the Dietary Inflammatory Index (DII) provides a quantitative means for assessing the role of diet in relation to health outcomes. Objetive: this study aimed to assess the association between the inflammatory potential of diet, as measured by the DII and IL-17A levels in young adults. Methods: a cross-sectional study was conducted on 69 adults between 18-30 y of age in San Luis Potosi, Mexico. Fasting blood samples were collected to analyze lipid profile, glucose homeostasis, and IL-17A. Dietary intake was assessed using a 24-hour recall. DII scores were calculated from 19 available food parameters. Univariate linear regression models were estimated to evaluate the possible dependence of IL-17A levels (dependent variables) on some potential explicative variables such as anthropometric, clinical, biochemical, and dietary variables. Results: there was a high inflammatory potential, with a mean DII score of +1.04 (range: -2.19 to +2.78). The DII was not associated with BMI, IL-17A levels or cardiometabolic risk factors. Conclusion: the study shows that the diets of healthy college-aged Mexican adults had a high inflammatory potential.

Lipid deposition is related to agricultural animal production and human health, and elucidating its molecular regulatory mechanisms is a topic of interest and a challenge in current scientific research. Musculoskeletal embryonic nuclear protein 1 (MUSTN1) regulates growth and development, including muscle tissue; however, its role in fat deposition remains unknown. Thus, our objective was to determine this role. Our new findings were as follows: MUSTN1 was highly expressed in the fat tissue of pigs with strong adipose deposition capacity; functionally, MUSTN1 promoted the proliferation and adipogenic differentiation of porcine and mouse preadipocytes. MUSTN1 knockout mice were protected against HFD-induced obesity, hepatic steatosis, and insulin resistance; and fatty acid binding protein 3 was identified as an interacting protein of MUSTN1, which facilitated preadipocyte proliferation and differentiation by activating the phosphatidylinositol 3 kinase/AKT signaling pathways. This study reveals a positive regulator for fat development, which suggests a novel approach for studying obesity and animal genetic improvement through the modulation of MUSTN1 expression.

Background: Obese adipose tissue produces various pro-inflammatory cytokines that are major contributors to adipose tissue inflammation.

Objective: The present study aimed to determine the effects of HM-chromanone (HMC) against obesity and adipose tissue inflammation in high-fat diet-fed mice.

Materials and methods: Twenty-four C57BL/6J male mice were divided into three groups: ND (normal diet), HFD (high-fat diet), and HFD + HMC. The ND group was fed a normal diet, whereas the HFD and HFD + HMC groups were fed a high-fat diet. After 10 weeks of feeding, the animals were orally administered the treatments daily for 9 weeks. The ND and HFD group received distilled water as treatment. The HFD+HMC group was treated with HM-chromaone (50 mg/kg).

Results: HM-chromanone administration decreased body weight, fat mass, and adipocyte diameter. HM-chromanone also improved plasma lipid profiles, decreased leptin levels, and increased adiponectin levels. The inhibiting effect of HM-chromanone on SREBP-1c, PPARγ, C/EBPα, and FAS decreased adipogenesis, thereby alleviating lipid accumulation. Furthermore, HM-chromanone administration exhibited a reduction in macrophage infiltration and the expression of pro-inflammatory cytokines. HM-chromanone suppressed the phosphorylation of IκBα and NF-κB, leading to the inhibition of iNOS and COX2 expressions, resulting in decreased inflammation in adipose tissue.

Discussion and conclusion: These results highlight the anti-obesity and anti-inflammatory properties of HM-chromanone, achieved through the downregulation of the SREBP-1c and NF-κB pathway in high-fat diet-fed mice.

To assess the relationship between body composition indicators and inflammatory biomarkers in children and adolescents of the GENOBOX study.

Anthropometry data from 264 subjects from the subsample of Zaragoza (Spain) included: weight, height, waist circumference, body mass index and triponderal index. Body composition was determined by Dual-energy X-ray Absorptiometry (DXA), obtaining visceral adipose tissue, fat mass index and lean mass index. Age and sex specific z-scores were computed. Simple linear regression models were performed with inflammatory biomarkers (hsCRP, IL8, TNF-α, adiponectin, leptin and resistin) as dependent variables, and each of the body composition indices as independent variables. Prepubertal boys had higher IL8 and resistin values and pubertal girls had higher HOMA-IR and leptin values. hsCPR and leptin were associated with fat mass, both in prepubertals and pubertals, independently of lean mass, and regardless of how body composition was measured. All body composition indices were inversely associated with adiponectin, except for fat mass index in pubertals, but none of them were statistically significant.

A positive association between hsCRP and leptin with all body fat composition parameters, measured by standard nutritional indicators and DXA, was observed in both sexual stages.

Food allergy is defined as an abnormal immune system response to the ingestion of certain ingredients or food additives. Beta-glucans may support the management of obesity, particularly due to their immunomodulatory properties. However, the possible adverse reactions of this nutraceutical are little known. This report documents an allergic skin reaction in a 6-year-old obese mixed-breed dog after consuming 0.1% purified beta-1,3/1,6-glucans from Saccharomyces Cerevisiae and subsequent dermatological signs after ingesting beta-1,3-glucans from Euglena gracilis. The dog was enrolled in a clinical trial designed to evaluate the effects of two types of beta-glucans on digestive, immunological, and intestinal health in obese dogs. Three nutritionally similar extruded dry diets were utilized: a control (CTL) diet without beta-glucans, beta-glucan A (BGA) containing 0.1% beta-1,3/1,6-glucans, and beta-glucan B (BGB) with 0.1% beta-1,3-glucans. Initially, the dog was deemed healthy, with all clinical parameters being within normal ranges. After a 30-day adaptation period consuming the CTL diet, the dog was randomized to the BGA diet. Within 30 days, the owner reported intense pruritus, alopecia, and erythema in various areas. A nutritional consultation confirmed that the dog had never been exposed to beta-glucans before. The CTL diet was reinstated, resulting in symptom resolution within 1 week. Following a subsequent challenge with the BGA diet, dermatological manifestations reemerged after 14 days but again resolved after returning to the CTL diet. The owner then agreed to a challenge with the BGB diet, leading to the reappearance of clinical signs after 15 days. The CTL diet was reintroduced, resulting in symptom resolution within ten days. However, the owner declined further testing with the BGB diet. This case concludes that the dog exhibited allergic reactions to purified beta-1,3/1,6-glucans from Saccharomyces cerevisiae, while reactions to Euglena gracilis, although highly probable, remain unconfirmed due to the lack of a provocation test.

Obesity and obesity-related metabolic diseases are causally linked to inflammatory activation. Proinflammatory macrophage infiltration and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome activation contribute to chronic inflammation and insulin resistance. Alleviating inflammatory responses is a reliable method to restore insulin sensitivity and reduce the severity of metabolic syndrome. Solanesol, rich in anti-inflammatory foods (potato, tomato, eggplant, chili peppers), has demonstrated anti-inflammatory properties, but whether it plays a beneficial role in obesity-induced chronic inflammation remains poorly understood. In this study, we investigated the effects of solanesol on the NLRP3 inflammasome and inflammatory responses both in vitro and in high-fat diet (HFD)-fed mice. We found that oral administration of solanesol reduced weight gain, insulin resistance, and inflammation in epididymal white adipose tissue (eWAT) in both HFD-fed obese mice and mice concurrently treated with a HFD. This effect was involved with reducing macrophage inflammation and inactivating the NLRP3 inflammasome by reducing the K+ efflux and reactive oxygen species (ROS) production in macrophages. Solanesol also reprogrammed the phenotype of inflammatory macrophages. Taken together, our study suggests that solanesol may be a promising candidate for treating obesity and obesity-related metabolic diseases.

Obesity-induced bone loss affects the life quality of patients all over the world. Irisin, one of the myokines, plays an essential role in bone and fat metabolism.

Investigate the effects of irisin on bone metabolism via adipocytes in the bone marrow microenvironment.

In this study, we fed fibronectin type III domain-containing protein 5 (FNDC5, the precursor protein of irisin) knockout mice (FNDC5-/-) with a high-fat diet (HFD) for 10 weeks. The quality of bone mass was assessed by micro-CT analysis, histological staining, and dynamic bone formation. In vitro, the lipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) was assayed by Oil Red O staining, and the osteogenic differentiation was assayed by alkaline phosphatase staining. Meanwhile, the gene expression in the BMSC-differentiated adipocytes by RNA sequence and the involved pathway of irisin were determined by western blot and qRT-PCR were performed.

The FNDC5-/- mice fed with a HFD showed an increased body weight, fat content of the bone marrow and bone, and a decreased bone formation compared with those with a standard diet (SD). In vitro, irisin inhibited the differentiation of BMSCs into adipocytes and alleviated the inhibition of osteogenesis derived from BMSCs by the adipocyte supernatant. RNA sequence and blocking experiment showed that irisin reduced the production of interleukin 6 (IL-6) in adipocytes through downregulating the TLR4/MyD88/NF-κB pathway. Immunofluorescence staining of bone marrow further confirmed an increased IL-6 expression in the FNDC5-/- mice fed with HFD compared with those fed with SD, which suffered serious bone loss.

Irisin downregulates activation of the TLR4/MyD88/NF-κB pathway, thereby reducing IL-6 production in adipocytes to enhance the osteogenesis of BMSCs. Thus, the rescue of osteogenesis of BMSCs, initially inhibited by IL-6, is a potential therapeutic target to mitigate obesity-induced osteoporosis.

Background and Objectives: This study aimed to evaluate serum asprosin levels in female patients with fibromyalgia syndrome (FM), investigate their associations with clinical parameters such as disease severity, anxiety, and depression, and evaluate the potential of serum asprosin levels as a biomarker for fibromyalgia diagnosis. Materials and Methods: A total of 80 participants were included in the study, 40 women aged 18-60 years who were diagnosed with FM according to the American College of Rheumatology (ACR) 2016 criteria and 40 healthy women with similar sociodemographic characteristics to the patient group. All participants were measured for hemograms, biochemistry tests, and serum asprosin levels. Additionally, the Fibromyalgia Impact Questionnaire (FIQ), Beck Anxiety Inventory (BAI), and Beck Depression Inventory (BDI) were administered to the patient group. Results: The median asprosin level in the case group was 15.01 (SD = 10.08-31.42), while in the control group it was 31.03 (SD = 25.14-35.7). The asprosin levels in the case group were significantly lower than those in the control group (p = 0.001). In contrast, AST, vitamin B12, and folic acid levels were significantly higher in the case group than in the control group. When all participants were evaluated, asprosin levels showed a significant positive correlation with systolic arterial blood pressure (Rho = 0.337, p = 0.002) and diastolic arterial blood pressure (Rho = 0.238, p = 0.033). A cut-off value of 17.72 ng/mL for asprosin levels in the diagnosis of fibromyalgia demonstrated a sensitivity of 60% and a specificity of 90%. Conclusions: Low asprosin levels may serve as a potential biomarker for the diagnosis of fibromyalgia in women.

Overweight patients with cardiovascular disease (CVD) tend to survive longer than normal-weight patients, a phenomenon known as the "obesity paradox". The phenotypic characteristics of adipose distribution in these patients (who survive longer) often reveal a larger proportion of subcutaneous white adipose tissue (scWAT), suggesting that the presence of scWAT is negatively associated with all-cause mortality and that scWAT appears to provide protective benefits in patients facing unhealthy states. Exercise-mediated browning is a crucial aspect of the benign remodeling process of adipose tissue (AT). Reduced accumulation, reduced inflammation, and associated adipokine secretion are directly related to the reduction in CVD mortality. This paper summarized the pathogenetic factors associated with AT accumulation in patients with CVD and analyzed the possible role and pathway of exercise-mediated adipose browning in reducing the risk of CVD and CVD-related mortality. It is suggested that exercise-mediated browning may provide a new perspective on the "obesity paradox"; that is, overweight CVD patients who have more scWAT may gain greater cardiovascular health benefits through exercise.

To compare radiographic measurements of lateral tibial slope (LTS), medial TS (MTS), and coronal TS (CTS) in MRI-defined intact, injured, and mucoid-degenerated native ACL knees and determine inter-reader reliability.

Patient records from 2 years at tertiary care hospitals were reviewed for individuals aged 18-100 undergoing 3-Tesla knee MRI and radiographs. Two randomly selected cohorts, control, and pathologic ACLs on MRI with 86 patients each, were age, gender, and BMI-matched. A fellowship-trained musculoskeletal radiologist reevaluated curated images, characterizing ACL status. Two trained medical students independently collected clinical data and measured slopes on blinded radiographs. ICC, Cohen's kappa, and case-control matching were performed using SPSS statistical package, with ICC and ANOVA used for comparisons.

Among 172 patients with 172 MRIs and radiographs, there were 86 controls and 86 ACL lesions. There were 108/172 (62.79%) males and 64/172 (37.21%) females. ICCs were 0.966 for MTS, 0.975 for LTS, and 0.978 for CTS. Mucoid degeneration patients had a higher BMI and were older than control (p < .05) or completely torn (p < .001) ACL patients. There was no difference in TS between normal and pathologic ACLs; however, LTS-MTS differences were larger with partial tears (2.5 ± 4.9) than normal ACLs by 4.5° (± 1.2, p < .001), complete tears by 4.5° (± 1.3, p < .001), and mucoid degeneration by 4.9° (± 1.5, p = .001).

Various TS measurements are reliable. LTS-MTS differences are associated with different ACL lesions compared to normal ACLs.

High scores of lymphocyte-to-high-density lipoprotein cholesterol ratio (lymphocyte-to-HDL-c) may be a new indicator of inflammation and metabolic syndrome. Here, we investigated the associations of the lymphocyte-to-HDL-c with traditional and non-traditional cardiometabolic risk markers in subjects at high cardiovascular risk. This study is a cross-sectional analysis with subjects assisted in a Secondary Health Care (n = 581, age = 63.06 ± 13.86 years; 52.3% women). Lymphocyte-to-HDL-c ratio were assessed by routine laboratory tests. Anthropometric and/or biochemical variables were used to calculate traditional (body mass index - BMI, and waist-to-height ratio - WHtR) and non-traditional (lipid accumulation product index-LAP, visceral adiposity index-VAI, deep-abdominal-adipose-tissue index-DAAT, atherogenic index of plasma-AIP, and waist-hypertriglyceridemic phenotype-HTGW) cardiometabolic risk markers. Furthermore, anthropometric measurement waist circumference (WC), blood pressure, metabolic syndrome (MS), and biochemical markers (lipid and glycemic profile) were considered traditional markers of cardiometabolic risk. Pearson's chi-square test, Poisson regression with robust variance, or multinomial logistic regression were performed (α = 0.05). Individuals with a high lymphocyte-HDL-c ratio (> 0.84, 3rd tertile) were associated with the HTGW phenotype, high VAI, high LAP, hypertriglyceridemia, high AIP, high very low-density lipoprotein-cholesterol (VLDL-c), pre-diabetes, and 3 and 4 MS components compared with individuals in the first tertile, independent of confounders. Our findings supported the lymphocyte-to-HDL-c ratio as a potential biomarker during the screening of subjects at high cardiovascular risk.

Asthma is a heterogeneous, multifactorial disease with multiple genetic and environmental risk factors playing a role in pathogenesis and therapeutic response. Understanding of pharmacogenetics can help with matching individualized treatments to specific genotypes of asthma to improve therapeutic outcomes especially in uncontrolled or severe asthma.

In this review, we outline novel information about biology, pathways, and mechanisms related to interindividual variability in drug response (corticosteroids, bronchodilators, leukotriene modifiers, and biologics) for childhood asthma. We discuss candidate gene, genome-wide association studies and newer omics studies including epigenomics, transcriptomics, proteomics, and metabolomics as well as integrative genomics and systems biology methods related to childhood asthma. The articles were obtained after a series of searches, last updated November 2022, using database PubMed/CINAHL DB.

Implementation of pharmacogenetic algorithms can improve therapeutic targeting in children with asthma, particularly with severe or uncontrolled asthma who typically have challenges in clinical management and carry considerable financial burden. Future studies focusing on potential biomarkers both clinical and pharmacogenetic can help formulate a prognostic test for asthma treatment response that would represent true bench to bedside clinical implementation.

Triglyceride (TG) metabolism is a complex and highly coordinated biological process regulated by a series of genes, and its dysregulation can lead to the occurrence of disorders in lipid metabolism. However, the transcriptional regulatory mechanisms of crucial genes in TG metabolism mediated by enhancer-promoter interactions remain elusive. Here, we identified candidate enhancers regulating the Agpat2, Dgat1, Dgat2, Pnpla2, and Lipe genes in 3T3-L1 adipocytes by integrating epigenomic data (H3K27ac, H3K4me1, and DHS-seq) with chromatin three-dimensional interaction data. Luciferase reporter assays revealed that 11 enhancers exhibited fluorescence activity. The repression of enhancers using the dCas9-KRAB system revealed the functional roles of enhancers of Dgat2 and Pnpla2 in regulating their expression and TG metabolism. Furthermore, transcriptome analyses revealed that inhibition of Dgat2-En4 downregulated pathways associated with lipid metabolism, lipid biosynthesis, and adipocyte differentiation. Additionally, overexpression and motif mutation experiments of transcription factor found that two TFs, PPARG and RXRA, regulate the activity of Agpat2-En1, Dgat2-En4, and Pnpla2-En5. Our study identified functional enhancers regulating TG metabolism and elucidated potential regulatory mechanisms of TG deposition from enhancer-promoter interactions, providing insights into understanding lipid deposition.

The current study was designed with the aim of conducting a systematic review and meta-analysis to determine the circulating levels of visfatin in patients with chronic obstructive pulmonary disease (COPD) compared to healthy individuals.

Until March 2024, we searched the Web of Science, PubMed/Medline, and Scopus databases. The analysis included case-control studies assessing the association between circulating visfatin and COPD. The random effects model was utilized to analyse the results with the help of Standard Mean of Differences (SMD) and 95% confidence interval (CI). The heterogeneity of the data was assessed using Cochrane Q and I2 values.

Seven studies were eligible to be included in the meta-analysis, with the COPD and healthy (control) groups having 265 and 244 subjects, respectively. The pooled results showed that although the circulating concentration of visfatin was lower in patients with COPD, no significant difference was observed (SMD: -0.48 mg/L; 95% CI: -1.67 to 0.70; p = 0.43). Subgroup analysis revealed that visfatin levels were significantly reduced in FEV1 less than 50% (p < 0.001) and in GOLD grade I-II (p < 0.05). Visfatin was shown to be significantly associated with IL-6 (p < 0.001) and TNF-α (p < 0.01) in the correlation meta-analysis. Meta-regression analysis revealed a significant correlation between the pooled SMD visfatin and pooled SMD age (p < 0.01), BMI (p < 0.001), FEV1 (p < 0.001), and IL-6 (p < 0.001).

The findings showed an insignificant decline in visfatin level among COPD patients, but additional research is necessary due to the heterogeneity in study results.

PROSPERO (CRD42023450851), https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023450851.

Sarcopenia is defined as a muscle-wasting syndrome that occurs with accelerated aging, while cachexia is a severe wasting syndrome associated with conditions such as cancer and immunodeficiency disorders, which cannot be fully addressed through conventional nutritional supplementation. Sarcopenia can be considered a component of cachexia, with the bidirectional interplay between adipose tissue and skeletal muscle potentially serving as a molecular mechanism for both conditions. However, the underlying mechanisms differ. Recognizing the interplay and distinctions between these disorders is essential for advancing both basic and translational research in this area, enhancing diagnostic accuracy and ultimately achieving effective therapeutic solutions for affected patients. This review discusses the muscle microenvironment's changes contributing to these conditions, recent therapeutic approaches like lifestyle modifications, small molecules, and nutritional interventions, and emerging strategies such as gene editing, stem cell therapy, and gut microbiome modulation. We also address the challenges and opportunities of multimodal interventions, aiming to provide insights into the pathogenesis and molecular mechanisms of sarcopenia and cachexia, ultimately aiding in innovative strategy development and improved treatments.

Obesity is commonly linked to both adenotonsillar hypertrophy (ATH) and allergic disorders, in which the roles of adipokines are not fully illuminated. This study aims to investigate the levels of leptin and adiponectin and their associations with allergic sensitization in pediatric ATH.

Serum levels of specific immunoglobulin E (IgE), leptin and adiponectin were quantified in 35 controls and 111 ATH children, in which 54 were non-atopic and 57 were atopic. Spearman's correlation analysis and polynomial linear trend test were conducted. The odds ratios and 95% confidence intervals were calculated by binary logistic regression after multivariable adjustment.

The serum level of leptin and leptin/adiponectin (L/A) ratio was significantly increased in children with ATH. An increase in leptin level and L/A ratio and a decrease in adiponectin level were observed in atopic children compared with non-atopic children. Among ATH children, the level of adiponectin was negatively while L/A ratio was positively correlated with specific IgE. After multivariable adjustment, leptin was significantly associated with increased risk of atopy to D. pteronyssinus and D. farina, and adiponectin was significantly associated with decreased risk of atopy to willow and mugwort. Leptin was associated with higher odds while adiponectin was associated with lower odds of overall atopy. Besides, significant multiplicative interactions of obesity with leptin and adiponectin on atopy were observed respectively.

Leptin and adiponectin were both associated with allergic sensitization and function differently in pediatric ATH. Mechanistic studies are needed to elucidate the involvement of adipokines in allergic sensitization of pediatric ATH.

Obesity is a global health concern that increases the risk of numerous complications, including type 2 diabetes, hypertension, and cardiovascular diseases. Conventional obesity treatments, such as lifestyle modifications, pharmacotherapy, and surgical interventions, are often insufficient, highlighting the need for more efficient and effective approaches. Yoga, an ancient mind-body practice incorporating physical postures (asanas), breathing exercises (pranayama), and meditation, has emerged as a potential therapeutic intervention for obesity management. This review examines the functions of leptin and adiponectin, two key adipocytokines central to obesity, and evaluates the impact of yoga on these hormones. A literature search was conducted using PubMed, Scopus, and Google Scholar with the keywords "yoga" and "adipocytokine" as of May 5, 2024, resulting in the selection of 12 relevant studies. The majority of studies reviewed demonstrated that yoga significantly decreases leptin levels and increases adiponectin levels. Intensive yoga sessions and combined dietary interventions were found to contribute notably to improvements in these hormonal levels. These findings suggest that yoga may improve the balance between leptin and adiponectin, offering beneficial effects on anti-obesity and chronic inflammation reduction. Yoga, as an economical and non-invasive treatment option, presents a promising approach to managing obesity. Further research is expected to elucidate the underlying mechanisms and explore potential clinical applications.

Bronchopulmonary dysplasia (BPD) is a chronic lung disease in premature infants caused by an imbalance between lung injury and lung repair in the developing immature lungs of the newborn. Pulmonary inflammation is an important feature in the pathogenesis of BPD. The aim of this study was to evaluate the relationship between the inflammatory microenvironment and the levels of visfatin and nesfatin-1, which are among the new adipocytokines, in BPD patients.

The groups consisted of 30 patients with BPD and 30 healthy children. Plasma levels of visfatin and nesfatin-1 and inflammation-related markers including interleukin-4 (IL-4), interleukin-10 (IL-10), nuclear factor kappa B (Nf-κB) and matrix metalloproteinase-9 (MMP-9) were determined by enzyme-linked immunosorbent assay (ELISA). RT-PCR was performed to evaluate the change in mRNA expression of visfatin and nesfatin-1 in the groups.

Visfatin levels were significantly higher in the BPD group compared to the healthy control (7.05±4.07 ng/ml vs. 2.13±1.66 ng/ml, p<0.0001). There was a 1.36±0.12 fold increase in visfatin mRNA expression (p<0.05) in the BPD group. There was no significant difference in plasma levels of nesfatin-1, IL-4, and IL-10 between the groups. Although MMP-9 and Nf-κB levels were significantly higher in the BPD group (p<0.0001), there was no correlation between visfatin levels and MMP-9 and Nf-κB levels in BPD patients.

This study showed that significant changes in visfatin levels in BPD patients might be associated with the risk of developing inflammation in BPD.

Sarcoidosis is a chronic disease of unknown etiology characterised by systemic non-caseating granulomas that can affect any organ in the body, especially the lungs and in which genetic and environmental factors are thought to play a role in its pathophysiology. Adipokines and myokines secreted from adipose and muscle tissue play a role in the pathogenesis or protection against many inflammatory and autoimmune diseases in which inflammation and immunity form the basis. In our study, we aimed to investigate the role of the irisin and adiponectin in sarcoidosis.

The study included 90 sarcoidosis patients and 86 healthy subjects. Adiponectin and irisin levels were analysed in addition to standard tests for diagnosis and follow-up of patients with sarcoidosis. The sensitivity and specificity of serum irisin levels for the diagnosis of sarcoidosis were evaluate dusing ROC analysis.

Irisin levels were significantly lower in the patient group than in the control group (3.28-5.25, p < 0.001). There was no association between irisin levels and extrapulmonary involvement. The cut-off irisin value for the diagnosis of sarcoidosis was ≤ 4.2662 with 95% confidence interval, and the sensitivity and specificity were calculated as 84% and 55.8%, respectively.

To our knowledge, this is the first study to investigate irisin in sarcoidosis patients. Based on the available evidence, anti-inflammatory, anti-oxidant and anti-apoptocic effects of irisin may play a role in the pathophysiology of sarcoidosis. Although no significant difference was found in our study, we believe that a comprehensive evaluation of adiponectin in sarcoidosis is important.

Recent insights into the influence of nutrition on immune system components have driven the development of dietary strategies targeting the prevention and management of major metabolic-inflammatory diseases. This review summarizes the bidirectional relationship between nutrition and immunocompetence, beginning with an overview of immune system components and their functions. It examines the effects of nutritional status, dietary patterns, and food bioactives on systemic inflammation, immune cell populations, and lymphoid tissues, as well as their associations with infectious and chronic disease pathogenesis. The mechanisms by which key nutrients influence immune constituents are delineated, focusing on vitamins A, D, E, C, and B, as well as minerals including zinc, iron, and selenium. Also highlighted are the immunomodulatory effects of polyunsaturated fatty acids as well as bioactive phenolic compounds and probiotics, given their expanding relevance. Each section addresses the implications of nutritional and nutraceutical interventions involving these nutrients within the broader context of major infectious, metabolic, and inflammatory diseases. This review further underscores that, while targeted nutrient supplementation can effectively restore immune function to optimal levels, caution is necessary in certain cases, as it may increase morbidity in specific diseases. In other instances, dietary counseling should be integrated to ensure that therapeutic goals are achieved safely and effectively.

Knee osteoarthritis (OA) is a major public health issue causing chronic pain, impaired physical function, and reduced quality of life. As there is no cure, self-management of symptoms via exercise is recommended by all current international clinical guidelines. This review updates one published in 2015.

We aimed to assess the effects of land-based exercise for people with knee osteoarthritis (OA) by comparing: 1) exercise versus attention control or placebo; 2) exercise versus no treatment, usual care, or limited education; 3) exercise added to another co-intervention versus the co-intervention alone.

We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, Embase, and two trial registries (ClinicalTrials.gov and World Health Organisation International Clinical Trials Registry Platform), together with reference lists, from the date of the last search (1st May 2013) until 4 January 2024, unrestricted by language.

We included randomised controlled trials (RCTs) that evaluated exercise for knee OA versus a comparator listed above. Our outcomes of interest were pain severity, physical function, quality of life, participant-reported treatment success, adverse events, and study withdrawals.

We used the standard methodological procedures expected by Cochrane for systematic reviews of interventions.

We included 139 trials (12,468 participants): 30 (3065 participants) compared exercise to attention control or placebo; 60 (4834 participants) compared exercise with usual care, no intervention or limited education; and 49 (4569 participants) evaluated exercise added to another intervention (e.g. weight loss diet, physical therapy, detailed education) versus that intervention alone. Interventions varied substantially in duration, ranging from 2 to 104 weeks. Most of the trials were at unclear or high risk of bias, in particular, performance bias (94% of trials), detection bias (94%), selective reporting bias (68%), selection bias (57%), and attrition bias (48%). Exercise versus attention control/placebo Compared with attention control/placebo, low-certainty evidence indicates exercise may result in a slight improvement in pain immediately post-intervention (mean 8.70 points better (on a scale of 0 to 100), 95% confidence interval (CI) 5.70 to 11.70; 28 studies, 2873 participants). Moderate-certainty evidence indicates exercise likely results in an improvement in physical function (mean 11.27 points better (on a scale of 0 to 100), 95% CI 7.64 to 15.09; 24 studies, 2536 participants), but little to no improvement in quality of life (mean 6.06 points better (on a scale of 0 to 100), 95% CI -0.13 to 12.26; 6 studies, 454 participants). There was moderate-certainty evidence that exercise likely increases participant-reported treatment success (risk ratio (RR) 1.46, 95% CI 1.11 to 1.92; 2 studies 364 participants), and likely does not increase study withdrawals (RR 1.08, 95% CI 0.92 to 1.26; 29 studies, 2907 participants). There was low-certainty evidence that exercise may not increase adverse events (RR 2.02, 95% CI 0.62 to 6.58; 11 studies, 1684 participants). Exercise versus no treatment/usual care/limited education Compared with no treatment/usual care/limited education, low-certainty evidence indicates exercise may result in an improvement in pain immediately post-intervention (mean 13.14 points better (on a scale of 0 to 100), 95% CI 10.36 to 15.91; 56 studies, 4184 participants). Moderate-certainty evidence indicates exercise likely results in an improvement in physical function (mean 12.53 points better (on a scale of 0 to 100), 95% CI 9.74 to 15.31; 54 studies, 4352 participants) and a slight improvement in quality of life (mean 5.37 points better (on a scale of to 100), 95% CI 3.19 to 7.54; 28 studies, 2328 participants). There was low-certainty evidence that exercise may result in no difference in participant-reported treatment success (RR 1.33, 95% CI 0.71 to 2.49; 3 studies, 405 participants). There was moderate-certainty evidence that exercise likely results in no difference in study withdrawals (RR 1.03, 95% CI 0.88 to 1.20; 53 studies, 4408 participants). There was low-certainty evidence that exercise may increase adverse events (RR 3.17, 95% CI 1.17 to 8.57; 18 studies, 1557 participants). Exercise added to another co-intervention versus the co-intervention alone Moderate-certainty evidence indicates that exercise when added to a co-intervention likely results in improvements in pain immediately post-intervention compared to the co-intervention alone (mean 10.43 points better (on a scale of 0 to 100), 95% CI 8.06 to 12.79; 47 studies, 4441 participants). It also likely results in a slight improvement in physical function (mean 9.66 points better, 95% CI 7.48 to 11.97 (on a 0 to 100 scale); 44 studies, 4381 participants) and quality of life (mean 4.22 points better (on a 0 to 100 scale), 95% CI 1.36 to 7.07; 12 studies, 1660 participants) immediately post-intervention. There was moderate-certainty evidence that exercise likely increases participant-reported treatment success (RR 1.63, 95% CI 1.18 to 2.24; 6 studies, 1139 participants), slightly reduces study withdrawals (RR 0.82, 95% CI 0.70 to 0.97; 41 studies, 3502 participants), and slightly increases adverse events (RR 1.72, 95% CI 1.07 to 2.76; 19 studies, 2187 participants). Subgroup analysis and meta-regression We did not find any differences in effects between different types of exercise, and we found no relationship between changes in pain or physical function and the total number of exercise sessions prescribed or the ratio (between exercise group and comparator) of real-time consultations with a healthcare provider. Clinical significance of the findings To determine whether the results found would make a clinically meaningful difference to someone with knee OA, we compared our results to established 'minimal important difference' (MID) scores for pain (12 points on a 0 to 100 scale), physical function (13 points), and quality of life (15 points). We found that the confidence intervals of mean differences either did not reach these thresholds or included both a clinically important and clinically unimportant improvement.

We found low- to moderate-certainty evidence that exercise probably results in an improvement in pain, physical function, and quality of life in the short-term. However, based on the thresholds for minimal important differences that we used, these benefits were of uncertain clinical importance. Participants in most trials were not blinded and were therefore aware of their treatment, and this may have contributed to reported improvements.

Previous research has suggested a correlation between fine particulate matter (PM2.5) and type 2 diabetes mellitus (T2DM). However, the causality was vulnerable to confounding variables.

A two-sample multivariable mendelian randomization study was designed to examine the causal connection between PM2.5 and T2DM. PM2.5 trait was investigated as exposure while T2DM-related traits as outcomes. The summary data were obtained from the Finngen database and the open genome-wide association study database. The mendelian randomization estimates were obtained using the inverse-variance weighted approach, and multiple sensitivity analyses were conducted. There were potential causal relationships between PM2.5 and T2DM (OR = 2.418; P = 0.019), PM2.5 and glycated hemoglobin (HbA1c) (OR = 1.590; P = 0.041), and PM2.5 and insulin metabolism. PM2.5 was found to have no causal effect on fasting glucose and insulin, 2-h glucose, and insulin-like growth factor binding protein-1 (P > 0.05), while had a potential protective effect against some diabetes complications.

Our findings indicated potential causal relationships among PM2.5 and T2DM, especially the causal relationship between PM2.5 and long-term glucose levels.

This study explored how the weight-adjusted waist index (WWI) and a body shape index (ABSI) are related to serum neurofilament light chain (sNfL) levels among U.S. adults. We aimed to evaluate sNfL, which plays key roles in neuronal injury in neurological diseases, given its understudied connection to obesity.

We used cross-sectional data from the 2013-2014 National Health and Nutrition Examination Survey (NHANES) of people with complete information on the weight-adjusted waist index (WWI), a body shape index (ABSI), and serum neurofilament light chain (sNfL). Multiple linear regression analysis allowed us to investigate the separate connections among the WWI, ABSI, and sNfL. Moreover, interaction testing and subgroup analysis were performed to improve the general validity of our results. To assess any nonlinear correlations, we also performed threshold effect analysis and smoothed curve fitting.

WWI and ABSI were positively linked with sNfL (WWI: β = 0.05, 95% CI 0.01-0.09; ABSI: β = 1.65, 95% CI 3.53-13.72). There was no clear reliance on this association according to subgroup analysis and interaction tests. Smoothed curve fitting and saturation effects also demonstrated nonlinear associations between WWI and ABSI and sNfL, with inflection points of 10.38 and 0.38, respectively.

In the adult American population, while the WWI and ABSI are linearly positively correlated with serum neurofilament light protein (sNfL), the effect size is greater for the ABSI. This correlation provides fresh evidence connecting obesity to neurological conditions, deepening our comprehension of the extensive health impacts associated with obesity. Level of Evidence Level I, experimental studies.

Being born either small for gestational age (SGA) or large for gestational age (LGA) and experiencing rapid or slow growth after birth are associated with later-life obesity. Understanding the associations of dietary quality during pregnancy with infant growth may inform obesity prevention strategies.

To evaluate the associations of prenatal dietary quality according to the Healthy Eating Index (HEI) and the Empirical Dietary Inflammatory Pattern (EDIP) with infant size at birth and infant growth from birth to age 24 months.

This cohort study used data from birthing parent-child dyads in 8 cohorts participating in the Environmental influences on Child Health Outcomes program between 2007 and 2021. Data were analyzed from March 2021 to August 2024.

The HEI and the EDIP dietary patterns.

Outcomes of interest were infant birth weight, categorized as SGA, reference range, or LGA, and infant growth from birth to ages 6, 12, and 24 months, categorized as slow growth (weight-for-length z score [WLZ] score difference <-0.67), within reference range (WLZ score difference -0.67 to 0.67), or rapid (WLZ score difference, >0.67).

The study included 2854 birthing parent-child dyads (median [IQR] maternal age, 30 [25-34] years; 1464 [51.3%] male infants). The cohort was racially and ethnically diverse, including 225 Asian or Pacific Islander infants (7.9%), 640 Black infants (22.4%), 1022 Hispanic infants (35.8%), 664 White infants (23.3%), and 224 infants (7.8%) with other race or multiple races. A high HEI score (>80), indicative of a healthier diet, was associated with lower odds of LGA (adjusted odds ratio [aOR], 0.88 [95% CI, 0.79-0.98]), rapid growth from birth to age 6 months (aOR, 0.80 [95% CI, 0.37-0.94]) and age 24 months (aOR 0.82 [95% CI, 0.70- 0.96]), and slow growth from birth to age 6 months (aOR, 0.65 [95% CI, 0.50-0.84]), 12 months (aOR, 0.74 [95% CI, 0.65-0.83]), and 24 months (OR, 0.65 [95% CI, 0.56-0.76]) compared with an HEI score 80 or lower. There was no association between high HEI and SGA (aOR, 1.14 [95% CI, 0.95-1.35]). A low EDIP score (ie, ≤63.6), indicative of a less inflammatory diet, was associated with higher odds of LGA (aOR, 1.24 [95% CI, 1.13-1.36]) and rapid infant growth from birth to age 12 months (aOR, 1.50 [95% CI, 1.18-1.91]) and lower odds of rapid growth to age 6 months (aOR, 0.77 [95% CI, 0.71-0.83]), but there was no association with SGA (aOR, 0.80 [95% CI, 0.51-1.25]) compared with an EDIP score of 63.6 or greater.

In this cohort study, a prenatal diet that aligned with the US Dietary Guidelines was associated with reduced patterns of rapid and slow infant growth, known risk factors associated with obesity. Future research should examine whether interventions to improve prenatal diet are also beneficial in improving growth trajectory in children.

Leptin, a hormone secreted by adipose tissue, plays a pivotal role in maintaining energy metabolism and bone quality. Dysregulation of leptin can lead to the development of various pathological conditions. For example, the concentration of leptin is increased in individuals with obesity, and this increased concentration is positively correlated with higher bone mass. In addition, mice lacking leptin or the leptin receptor exhibit substantial bone loss, further highlighting the pivotal role of leptin in regulating bone metabolism. However, the precise mechanism through which leptin affects bone remodeling remains unclear. The present study investigated the effect of leptin on osteoclastogenesis and osteoblastogenesis. Osteoblasts derived from MC3T3-E1 cells and osteoclasts derived from RAW 264.7 cells were used. The findings revealed that leptin did not substantially affect osteoclastogenesis or osteoblastogenesis. Furthermore, leptin did not affect cell viability during osteoclast differentiation. The expression of inflammatory mediators was increased in differentiating RAW 264.7 cells. However, the expression of critical bone resorptive genes, including Ctsk and tartrate-resistant acid phosphatase, was not elevated following leptin stimulation. By contrast, leptin did not alter the expression of key osteogenic genes in preosteoblasts in the early stage of differentiation. These data demonstrate that leptin can stimulate the expression of pro-inflammatory mediators in differentiating osteoclasts. These changes do not affect osteoblastogenesis or osteoclastogenesis. Leptin may downregulate bone resorption and enhance mineralization to increase bone mass.

The global obesity epidemic, attributed to sedentary lifestyles, unhealthy diets, genetics and environmental factors, has led to over 1.9 billion adults being classified as overweight and 650 million living with obesity. Despite advancements in early detection and treatment, lung cancer prognosis remains poor due to late diagnoses and limited therapies. The obesity paradox challenges conventional thinking by suggesting that individuals with obesity and certain diseases, including cancer, may have an improved prognosis compared with their counterparts of a normal weight. This observation has prompted investigations to understand protective mechanisms, including potentially favorable adipokine secretion and metabolic reserves that contribute to tolerating cancer treatments. However, understanding the association between obesity and lung cancer is complex. While smoking is the primary risk factor of lung cancer, obesity may independently impact lung cancer risk, particularly in non‑smokers. Adipose tissue dysfunction, including low‑grade chronic inflammation, and hormonal changes contribute to lung cancer development and progression. Obesity‑related factors may also influence treatment responses and survival outcomes in patients with lung cancer. The impact of obesity on treatment modalities such as chemotherapy, radiotherapy and surgery is still under investigation. Challenges in managing patients with obesity and cancer include increased surgical complexity, higher rates of postoperative complications and limited treatment options due to comorbidities. Targeted interventions aimed at reducing obesity prevalence and promoting healthy lifestyles are crucial for lung cancer prevention. The impact of obesity on lung cancer is multifaceted and requires further research to elucidate the underlying mechanisms and develop personalized interventions for prevention and treatment.

Metabolic syndrome (MetS) is associated with the development of several diseases. However, the correlation between MetS and size of renal cysts remains unclear. This research aims to explore the potential connection between them, offering theoretical guidance for clinical prevention and treatment of renal cysts.

A total of 467 patients diagnosed with renal cysts and admitted to Sir Run Run Hospital, Nanjing Medical University from September 2019 to September 2020 were eventually included in this study. They were divided into the small cyst group (cyst volume≤1.5cm³) and the large cyst group (cyst volume>1.5cm³) based on the median value of cyst volume. Multivariate logistic regression analysis was used to evaluate the association between MetS and size of renal cysts.

Our results indicated that MetS (OR 1.941, 95% CI 1.286-2.927, P=0.002) was positively associated with the size of renal cysts. Additionally, multiple renal cysts (OR 2.259, 95% CI 1.402-3.640, P=0.001) and serum globulin (OR 0.945, 95% CI 0.905-0.987, P=0.011) were positively and negatively related to size of renal cysts, respectively.

Our study reveals the association between MetS and the size of renal cysts. Patients with MetS are more likely to have larger renal cysts. The administration of MetS may help limit the development of renal cysts. Further prospective studies are needed to explore the causal relationship between MetS and renal cysts.

Background/Objectives: The negative energy balance activaties of spontaneous lipolysis. This may promotes inflammation within the adipose tissue. The aim of the study was to explain the development of inflammation during increased lactogenesis. It was hypothesized that lipolysis contributes synthesis of interleukin-6 and plasminogen. Methods: The study was in production conditions carried out using Holstein-Friesian cows. The period studied covered time of early lactation. Results: Up to the peak of lactation, milk yield strongly influenced the rate of loss of body condition. This had an impact on with the intensity of the release of the fatty acids. In both cases this relationships strengthened to the peak of production. Oobserved tendencies towards a decrease in the concentration of glucose and an increase in that of leptin. Loss of the body condition and the release of NEFA were were influencing to affect the blood concentrations of interleukin-6 and plasminogen. We have shown that IL-6 has a relatively strong correlation with the NEFA. They correlate with IL-6 independently of EB influence. This may suggest independent associations between these variables, which could potentially be applied in practice. Conclusions: The NEFA release in the long term can increase the inflammatory response within adipose tissue and can intensify the release of interleukin-6 and plasminogen. It is likely that in the initial stage of lactogenesis, the inflammatory process developing within adipose tissue is physiologically justified. Our results can provide background to this little-described area of research.

Steatotic liver diseases (SLD) are the principal worldwide cause of cirrhosis and end-stage liver cancer, affecting nearly a quarter of the global population. SLD includes metabolic dysfunction-associated alcoholic liver disease (MetALD) and metabolic dysfunction-associated steatotic liver disease (MASLD), resulting in asymptomatic liver steatosis, fibrosis, cirrhosis and associated complications. The immune processes include gut dysbiosis, adiposeliver organ crosstalk, hepatocyte death and immune cell-mediated inflammatory processes. Notably, various immune cells such as B cells, plasma cells, dendritic cells, conventional CD4+ and CD8+ T cells, innate-like T cells, platelets, neutrophils and macrophages play vital roles in the development of MetALD and MASLD. Immunological modulations targeting hepatocyte death, inflammatory reactions and gut microbiome include N-acetylcysteine, selonsertib, F-652, prednisone, pentoxifylline, anakinra, JKB-121, HA35, obeticholic acid, probiotics, prebiotics, antibiotics and fecal microbiota transplantation. Understanding the immunological mechanisms underlying SLD is crucial for advancing clinical therapeutic strategies.

Chemerin and resistin are adipokines studied as potential markers for early diagnosis and disease severity in patients with knee osteoarthritis (KOA) Therefore, we aimed to investigate the associations serum and synovial levels of chemerin and resistin with inflammatory parameters and ultrasonographic scores (US) in KOA individuals. Serum was collected from 28 patients with KOA and synovial fluid was obtained from 16 of them. Another 31 age and sex matched cases with no joint disease were included as healthy controls. Concentrations of chemerin, resistin, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) were determined with ELISA. Erythrocyte sedimentation rate (ESR), C-reactive protein, serum uric acid (UA) were measured in the patients group. Participants with KOA underwent US assessment using the Outcome Measures in Rheumatology (OMERACT) scores. Patients with KOA had statistically significant higher level of serum resistin than healthy controls [11.05 (3.78-24.13) ng/mL and 7.23 (3.83-12.19) respectively, p < 0.001]. A strong correlation was found between serum chemerin and ESR (r = 0.434, p = 0.021), uric acid (r = 0.573, p = 0.001) as well as the US (r=-0.872, p < 0.001). Serum resistin demonstrated significant association with TNF-alpha (r = 0.398, p = 0.044). In conclusion, both chemerin and resistin might contribute to inflammatory changes associated with KOA. Further studies are needed to elucidate their potential role in the pathogenesis of the disease.

Adipose tissue macrophages (ATMs) play important roles in maintaining adipose tissue homeostasis and orchestrating metabolic inflammation. Given the extensive functional heterogeneity and phenotypic plasticity of ATMs, identification of the authentically pathogenic ATM subpopulation under obese setting is thus necessitated. Herein, we performed single-nucleus RNA sequencing (snRNA-seq) and unraveled a unique maladaptive ATM subpopulation defined as ATF4hiPDIA3hiACSL4hiCCL2hi inflammatory and metabolically activated macrophages (iMAMs), in which PDIA3 is required for the maintenance of their migratory and pro-inflammatory properties. Mechanistically, ATF4 serves as a metabolic stress sensor to transcribe PDIA3, which then imposes a redox control on RhoA activity and strengthens the pro-inflammatory and migratory properties of iMAMs through RhoA-YAP signaling. Administration of Pdia3 small interfering RNA (siRNA)-loaded liposomes effectively repressed adipose inflammation and high-fat diet (HFD)-induced obesity. Together, our data support that strategies aimed at targeting iMAMs by suppressing PDIA3 expression or activity could be a viable approach against obesity and metabolic disorders in clinical settings.