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Lee MC, Hsu YJ, Sung HC, Wen YT, Wei L, Huang CC. Low Aerobic Capacity Accelerates Lipid Accumulation and Metabolic Abnormalities Caused by High-Fat Diet-Induced Obesity in Postpartum Mice. Nutrients 2022; 14:nu14183746. [PMID: 36145123 PMCID: PMC9502809 DOI: 10.3390/nu14183746] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/27/2022] [Revised: 09/02/2022] [Accepted: 09/06/2022] [Indexed: 11/26/2022] Open
Abstract
Women during pregnancy and postpartum show high rates of obesity and metabolic diseases, especially women with excessive caloric intake. In the past, it was proved that individuals with high intrinsic aerobic exercise capacities showed higher lipid metabolism and lower fat production than those with low intrinsic aerobic exercise capacities. The purpose of this study was to determine whether mice with the low-fitness phenotype (LAEC) were more likely to develop metabolic abnormalities and obesity under dietary induction after delivery, and if mice with a high-fitness phenotype (HAEC) had a protective mechanism. After parturition and weaning, postpartum Institute of Cancer Research (ICR) mice received dietary induction for 12 weeks and were divided into four groups (n = 8 per group): high-exercise capacity postpartum mice with a normal chow diet (HAEC-ND); high-exercise capacity postpartum mice with a high-fat diet (HAEC-HFD); low-exercise capacity postpartum mice with a normal chow diet (LAEC-ND); and low-exercise capacity postpartum mice with a high-fat diet (LAEC-HFD). Obesity caused by a high-fat diet led to decreased exercise performance (p < 0.05). Although there were significant differences in body posture under congenital conditions, the LAEC mice gained more weight and body fat after high-fat-diet intake (p < 0.05). Compared with HAEC-HFD, LAEC-HFD significantly increased blood lipids, such as total cholesterol (TC), triacylglycerol (TG), low-density lipoprotein (LDL) and other parameters (p < 0.05), and the content of TG in the liver, as well as inducing poor glucose tolerance (p < 0.05). In addition, after HFD intake, excessive energy significantly increased glycogen storage (p < 0.05), but the LAEC mice showed significantly lower muscle glycogen storage (p < 0.05). In conclusion, although we observed significant differences in intrinsic exercise capacity, and body posture and metabolic ability were also different, high-fat-diet intake caused weight gain and a risk of metabolic disorders, especially in postpartum low-fitness mice. However, HAEC mice still showed better lipid metabolism and protection mechanisms. Conversely, LAEC mice might accumulate more fat and develop metabolic diseases compared with their normal rodent chow diet (ND) control counterparts.
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Affiliation(s)
- Mon-Chien Lee
- Graduate Institute of Sports Science, National Taiwan Sport University, Taoyuan 333325, Taiwan
| | - Yi-Ju Hsu
- Graduate Institute of Sports Science, National Taiwan Sport University, Taoyuan 333325, Taiwan
| | - Hsin-Ching Sung
- Department of Anatomy, College of Medicine, Chang Gung University, Taoyuan 333323, Taiwan
- Aesthetic Medical Center, Department of Dermatology, Chang Gung Memorial Hospital, Taoyuan 333423, Taiwan
| | - Ya-Ting Wen
- Division of Neurosurgery, Department of Surgery, Wan Fang Hospital, Taipei Medical University, Taipei 116081, Taiwan
| | - Li Wei
- Division of Neurosurgery, Department of Surgery, Wan Fang Hospital, Taipei Medical University, Taipei 116081, Taiwan
- Graduate Institute of Injury Prevention and Control, Taipei Medical University, Taipei 110301, Taiwan
- Taipei Neuroscience Institute, Taipei Medical University, Taipei 110301, Taiwan
- Correspondence: (L.W.); (C.-C.H.); Tel.: +886-2-27361661 (ext. 6579) (L.W.); +886-3-328-3201 (ext. 2619) (C.-C.H.)
| | - Chi-Chang Huang
- Graduate Institute of Sports Science, National Taiwan Sport University, Taoyuan 333325, Taiwan
- Correspondence: (L.W.); (C.-C.H.); Tel.: +886-2-27361661 (ext. 6579) (L.W.); +886-3-328-3201 (ext. 2619) (C.-C.H.)
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de Souza ILL, Barros BC, Ferreira EDS, Queiroga FR, Vasconcelos LHC, Toscano LDLT, Silva AS, da Silva PM, Cavalcante FDA, da Silva BA. Supplementation with Spirulina platensis Prevents Damage to Rat Erections in a Model of Erectile Dysfunction Promoted by Hypercaloric Diet-Induced Obesity. Mar Drugs 2022; 20:md20080467. [PMID: 35892935 PMCID: PMC9332348 DOI: 10.3390/md20080467] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/01/2022] [Revised: 04/23/2022] [Accepted: 04/26/2022] [Indexed: 01/27/2023] Open
Abstract
Erectile dysfunction (ED) is the inability to achieve and/or maintain a penile erection sufficient for sexual satisfaction. Currently, many patients do not respond to the pharmacotherapy. The effects of a supplementation with Spirulina platensis, were evaluated in a model of ED induced by hypercaloric diet consumption. Wistar rats were divided into groups fed with standard diet (SD) or hypercaloric diet (HD) and supplemented with this alga at doses of 25, 50 or 100 mg/kg. Experimental adiposity parameters and erectile function were analyzed. In SD groups, Spirulina platensis reduced food intake, final body mass and adiposity index, and increased the total antioxidant capacity (TAC) of adipose tissue. However, no change was observed in erectile function. In the HD group, without Spirulina supplementation, a decrease in food intake was observed, in addition to an increase of final body mass, weight gain, adipose reserves, and adiposity index. Additionally, reduction in the number and increase in the latency of penile erection and adipose malondialdehyde levels, as well as a reduction in TCA was noted. Furthermore, cavernous contractility was increased, and the relaxing response was decreased. Interestingly, these deleterious effects were prevented by the algae at doses of 25, 50 and/or 100 mg/kg. Therefore, the supplementation with S. platensis prevents damages associated to a hypercaloric diet consumption and emerges as an adjuvant the prevention of ED.
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Affiliation(s)
- Iara Leão Luna de Souza
- Departamento de Ciências Biológicas e Saúde, Universidade Estadual de Roraima, Boa Vista 69306-530, RR, Brazil
- Curso de Farmácia, Centro Universitário Estácio da Amazônia, Boa Vista 69306-530, RR, Brazil
- Correspondence: ; Tel.: +55-83-98741-9057
| | - Bárbara Cavalcanti Barros
- Programa de Pós-graduação em Produtos Naturais e Sintéticos Bioativos, Centro de Ciências da Saúde, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil; (B.C.B.); (E.d.S.F.); (F.R.Q.); (L.H.C.V.); (F.d.A.C.); (B.A.d.S.)
| | - Elba dos Santos Ferreira
- Programa de Pós-graduação em Produtos Naturais e Sintéticos Bioativos, Centro de Ciências da Saúde, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil; (B.C.B.); (E.d.S.F.); (F.R.Q.); (L.H.C.V.); (F.d.A.C.); (B.A.d.S.)
| | - Fernando Ramos Queiroga
- Programa de Pós-graduação em Produtos Naturais e Sintéticos Bioativos, Centro de Ciências da Saúde, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil; (B.C.B.); (E.d.S.F.); (F.R.Q.); (L.H.C.V.); (F.d.A.C.); (B.A.d.S.)
| | - Luiz Henrique César Vasconcelos
- Programa de Pós-graduação em Produtos Naturais e Sintéticos Bioativos, Centro de Ciências da Saúde, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil; (B.C.B.); (E.d.S.F.); (F.R.Q.); (L.H.C.V.); (F.d.A.C.); (B.A.d.S.)
- Centro de Ciências da Saúde, Departamento de Fisiologia e Patologia, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil
| | - Lydiane de Lima Tavares Toscano
- Centro de Ciências da Saúde, Departamento de Educação Física, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil; (L.d.L.T.T.); (A.S.S.)
| | - Alexandre Sérgio Silva
- Centro de Ciências da Saúde, Departamento de Educação Física, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil; (L.d.L.T.T.); (A.S.S.)
| | - Patrícia Mirella da Silva
- Programa de Pós-graduação em Biologia Celular e Molecular, Centro de Ciências Exatas e da Natureza, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil;
| | - Fabiana de Andrade Cavalcante
- Programa de Pós-graduação em Produtos Naturais e Sintéticos Bioativos, Centro de Ciências da Saúde, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil; (B.C.B.); (E.d.S.F.); (F.R.Q.); (L.H.C.V.); (F.d.A.C.); (B.A.d.S.)
- Centro de Ciências da Saúde, Departamento de Fisiologia e Patologia, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil
| | - Bagnólia Araújo da Silva
- Programa de Pós-graduação em Produtos Naturais e Sintéticos Bioativos, Centro de Ciências da Saúde, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil; (B.C.B.); (E.d.S.F.); (F.R.Q.); (L.H.C.V.); (F.d.A.C.); (B.A.d.S.)
- Centro de Ciências da Saúde, Departamento de Ciências Farmacêuticas, Universidade Federal da Paraíba, João Pessoa 58051-900, PB, Brazil
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Postnatally induced metabolic and oxidative changes associated with maternal high-fat consumption were mildly affected by Quercetin-3-O-rutinoside treatment in rats. Heliyon 2021; 7:e06847. [PMID: 33997389 PMCID: PMC8102762 DOI: 10.1016/j.heliyon.2021.e06847] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/29/2020] [Revised: 01/05/2021] [Accepted: 04/14/2021] [Indexed: 11/30/2022] Open
Abstract
Oxidative stress is usually associated with prolonged intake of high-fat diet (HFD). However, little is known about the impact of maternal HFD on endogenous modulation of antioxidant-defence-enzyme-network, its link to adverse fetal growth and overall effects of Quercetin-3-o-rutinoside (QR) supplementation. Sprague-Dawley rats were initially assigned to normal diet (ND) or HFD for 8 weeks and mated. Post-conception, rats were further divided into four groups, of which two groups had diets supplemented with QR while others continued with their respective diets until delivery. Measurements include food and water consumption, physical parameters (body weight, body mass index (BMI) and fur appearance), oral glucose tolerance, lipid profiles, and placental/liver oxidative changes. We observed that water consumption was significantly increased in dams fed HFD without marked differences in food intake, body weight, BMI and glucose tolerance. Surprisingly, offspring of HFD-fed dams had reduced body weight marked by delayed fur appearance compared to the ND offspring. In dams, there were alterations in lipid profile. Lipid peroxidation was increased in the placenta and liver of gestational day (GD) 19 HFD-fed dams and their postnatal day (PND) 21 male offspring. There was evidence of HFD-induced nitrosative stress in dams and PND28 female offspring. Adaptive defence indicate decreased placenta and liver superoxide dismutase (SOD) levels as well as differential changes in total antioxidant capacity (TAC) and catalase (CAT) activity in HFD treated dams and their progenies. Overall, the results indicate that intrauterine metabolic alterations associated with maternal high-fat consumption may induce oxidative challenge in the offspring accompanied by mild developmental consequences, while QR supplementation has little or no beneficial effects.
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Jeon YB, Lee J, Chang HC. Characterization of juice fermented with Lactobacillus plantarum EM and its cholesterol-lowering effects on rats fed a high-fat and high-cholesterol diet. Food Sci Nutr 2019; 7:3622-3634. [PMID: 31763011 PMCID: PMC6848804 DOI: 10.1002/fsn3.1217] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/15/2019] [Revised: 07/15/2019] [Accepted: 07/24/2019] [Indexed: 11/11/2022] Open
Abstract
The aim of this study was to investigate the ability of Lactobacillus plantarum EM as a starter culture to control cabbage-apple juice fermentation and to explore the cholesterol-lowering effects of the fermented juice (EM juice) in rats. L. plantarum EM produced strong antimicrobial activities against bacteria and fungi, suppressing other microorganisms in the fermented juice, and was the dominant organism during fermentation and storage. The EM juice also showed strong and broad-spectrum antimicrobial activity. Rats fed a high-fat and high-cholesterol diet and administered EM juice showed significantly reduced total cholesterol (TC), triglyceride, and LDL-cholesterol levels, as well as a reduced atherogenic index, lower cardiac factors in serum, and lower TC levels in the liver, while total lipid and TC levels in the rat feces increased. Reverse transcription-polymerase chain reaction analysis revealed that the hepatic mRNA expression of HMG-CoA reductase decreased and the expressions of cholesterol 7α-hydroxylase and low-density lipoprotein receptor increased in rats administered EM juice. The effects of EM juice on rats included inhibition of cholesterol synthesis as well as enhancement of cholesterol uptake and cholesterol excretion. The results of this study indicate that the use of L. plantarum EM as a functional starter culture for juice fermentation exerts microbial control, enhances sanitary safety, and provides beneficial food effects against hypercholesterolemia.
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Affiliation(s)
- Yu Bin Jeon
- Department of Food and NutritionKimchi Research CenterChosun UniversityGwangjuRepublic of Korea
| | - Jae‐Joon Lee
- Department of Food and NutritionKimchi Research CenterChosun UniversityGwangjuRepublic of Korea
| | - Hae Choon Chang
- Department of Food and NutritionKimchi Research CenterChosun UniversityGwangjuRepublic of Korea
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Liu HY, Walden TB, Cai D, Ahl D, Bertilsson S, Phillipson M, Nyman M, Holm L. Dietary Fiber in Bilberry Ameliorates Pre-Obesity Events in Rats by Regulating Lipid Depot, Cecal Short-Chain Fatty Acid Formation and Microbiota Composition. Nutrients 2019; 11:nu11061350. [PMID: 31208043 PMCID: PMC6627426 DOI: 10.3390/nu11061350] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/08/2019] [Revised: 06/05/2019] [Accepted: 06/11/2019] [Indexed: 12/19/2022] Open
Abstract
Obesity is linked to non-alcoholic fatty liver disease and risk factors associated to metabolic syndrome. Bilberry (Vaccinium myrtillus) that contains easily fermentable fiber may strengthen the intestinal barrier function, attenuate inflammation and modulate gut microbiota composition, thereby prevent obesity development. In the current study, liver lipid metabolism, fat depot, cecal and serum short-chain fatty acids (SCFAs) and gut microbiome were evaluated in rats fed bilberries in a high-fat (HFD + BB) or low-fat (LFD + BB) setting for 8 weeks and compared with diets containing equal amount of fiber resistant to fermentation (cellulose, HFD and LFD). HFD fed rats did not obtain an obese phenotype but underwent pre-obesity events including increased liver index, lipid accumulation and increased serum cholesterol levels. This was linked to shifts of cecal bacterial community and reduction of major SCFAs. Bilberry inclusion improved liver metabolism and serum lipid levels. Bilberry inclusion under either LFD or HFD, maintained microbiota homeostasis, stimulated interscapular-brown adipose tissue depot associated with increased mRNA expression of uncoupling protein-1; enhanced SCFAs in the cecum and circulation; and promoted butyric acid and butyrate-producing bacteria. These findings suggest that bilberry may serve as a preventative dietary measure to optimize microbiome and associated lipid metabolism during or prior to HFD.
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Affiliation(s)
- Hao-Yu Liu
- Department of Medical Cell Biology, Uppsala University, 75123 Uppsala, Sweden.
| | - Tomas B Walden
- Department of Medical Cell Biology, Uppsala University, 75123 Uppsala, Sweden.
| | - Demin Cai
- Department of Biochemistry and Molecular Medicine, University of California at Davis, Sacramento, CA 95817, USA.
| | - David Ahl
- Department of Medical Cell Biology, Uppsala University, 75123 Uppsala, Sweden.
| | - Stefan Bertilsson
- Department of Ecology and Genetics, Limnology and Science for Life Laboratory, Uppsala University, 75236 Uppsala, Sweden.
| | - Mia Phillipson
- Department of Medical Cell Biology, Uppsala University, 75123 Uppsala, Sweden.
| | - Margareta Nyman
- Department of Food Technology, Engineering and Nutrition, Lund University, 22100 Lund, Sweden.
| | - Lena Holm
- Department of Medical Cell Biology, Uppsala University, 75123 Uppsala, Sweden.
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Park YM, Kanaley JA, Zidon TM, Welly RJ, Scroggins RJ, Britton SL, Koch LG, Thyfault JP, Booth FW, Padilla J, Vieira-Potter VJ. Ovariectomized Highly Fit Rats Are Protected against Diet-Induced Insulin Resistance. Med Sci Sports Exerc 2017; 48:1259-69. [PMID: 26885638 DOI: 10.1249/mss.0000000000000898] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
Abstract
INTRODUCTION In the absence of exercise training, rats selectively bred for high intrinsic aerobic capacity (high-capacity running (HCR)) are protected against ovariectomy (OVX)-induced insulin resistance (IR) and obesity compared with those bred for low intrinsic aerobic capacity (low-capacity running (LCR)). PURPOSE This study determined whether OVX HCR rats remain protected with exposure to high-fat diet (HFD) compared with OVX LCR rats. METHODS Female HCR and LCR rats (n = 36; age, 27-33 wk) underwent OVX and were randomized to a standard chow diet (NC, 5% kcal fat) or HFD (45% kcal fat) ad libitum for 11 wk. Total energy expenditure, resting energy expenditure, spontaneous physical activity (SPA), and glucose tolerance were assessed midway, whereas fasting circulating metabolic markers, body composition, adipose tissue distribution, and skeletal muscle adenosine monophosphate-activated protein kinase (AMPK), and mitochondrial markers were assessed at sacrifice. RESULTS Both HCR and LCR rats experienced HFD-induced increases in total and visceral adiposity after OVX. Despite similar gains in adiposity, HCR rats were protected from HFD-induced IR and reduced total energy expenditure observed in LCR rats (P < 0.05). This metabolic protection was likely attributed to a compensatory increase in SPA and associated preservation of skeletal muscle AMPK activity in HCR; however, HFD significantly reduced SPA and AMPK activity in LCR (P < 0.05). In both lines, HFD reduced citrate synthase activity, gene expression of markers of mitochondrial biogenesis (tFAM, NRF1, and PGC-1α), and protein levels of mitochondrial oxidative phosphorylation complexes I, II, IV, and V in skeletal muscle (all P < 0.05). CONCLUSION After OVX, HCR and LCR rats differentially respond to HFD such that HCR increase while LCR decrease SPA. This "physical activity compensation" likely confers protection from HFD-induced IR and reduced energy expenditure in HCR rats.
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Affiliation(s)
- Young-Min Park
- 1Nutrition and Exercise Physiology, University of Missouri, Columbia, MO; 2Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, MI; 3Department of Molecular Integrative Physiology, University of Kansas Medical Center, Kansas City, KS; 4Biomedical Sciences, University of Missouri, Columbia, MO; 5Child Health, University of Missouri, Columbia, MO; 6Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO
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Daltro PS, Barreto BC, Silva PG, Neto PC, Sousa Filho PHF, Santana Neta D, Carvalho GB, Silva DN, Paredes BD, de Alcantara AC, Freitas LAR, Couto RD, Santos RR, Souza BSF, Soares MBP, Macambira SG. Therapy with mesenchymal stromal cells or conditioned medium reverse cardiac alterations in a high-fat diet-induced obesity model. Cytotherapy 2017; 19:1176-1188. [PMID: 28801055 DOI: 10.1016/j.jcyt.2017.07.002] [Citation(s) in RCA: 18] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/15/2017] [Revised: 06/13/2017] [Accepted: 07/04/2017] [Indexed: 11/18/2022]
Abstract
BACKGROUND Obesity is associated with numerous cardiac complications, including arrhythmias, cardiac fibrosis, remodeling and heart failure. Here we evaluated the therapeutic potential of mesenchymal stromal cells (MSCs) and their conditioned medium (CM) to treat cardiac complications in a mouse model of high-fat diet (HFD)-induced obesity. METHODS After obesity induction and HFD withdrawal, obese mice were treated with MSCs, CM or vehicle. Cardiac function was assessed using electrocardiography, echocardiography and treadmill test. Body weight and biochemical parameters were evaluated. Cardiac tissue was used for real time (RT)-polymerase chain reaction (PCR) and histopathologic analysis. RESULTS/DISCUSSION Characterization of CM by protein array showed the presence of different cytokines and growth factors, including chemokines, osteopontin, cystatin C, Serpin E1 and Gas 6. HFD-fed mice presented cardiac arrhythmias, altered cardiac gene expression and fibrosis reflected in physical exercise incapacity associated with obesity and diabetes. Administration of MSCs or CM improved arrhythmias and exercise capacity. This functional improvement correlated with normalization of GATA4 gene expression in the hearts of MSC- or CM-treated mice. The gene expression of connexin 43, troponin I, adiponectin, transforming growth factor (TGF) β, peroxisome proliferator activated receptor gamma (PPARγ), insulin-like growth factor 1 (IGF-1), matrix metalloproteinase-9 (MMP9) and tissue inhibitor of metalloproteinases 1 (TIMP1) were significantly reduced in MSCs, but not in CM-treated mice. Moreover, MSC or CM administration reduced the intensity of cardiac fibrosis. CONCLUSION Our results suggest that MSCs and CM have a recovery effect on cardiac disturbances due to obesity and corroborate to the paracrine action of MSCs in heart disease models.
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Affiliation(s)
- P S Daltro
- Center for Biotechnology and Cell Therapy, Salvador, BA, Brazil; Multicentric Program in Biochemistry and Molecular Biology, Federal University of Bahia, Salvador, BA, Brazil
| | - B C Barreto
- Center for Biotechnology and Cell Therapy, Salvador, BA, Brazil; Faculty of Biology, Federal University of Bahia, Salvador, BA, Brazil
| | - P G Silva
- Faculty of Medicine, Federal University of Bahia, Salvador, BA, Brazil
| | - P Chenaud Neto
- Faculty of Medicine, Federal University of Bahia, Salvador, BA, Brazil
| | - P H F Sousa Filho
- Faculty of Medicine, Federal University of Bahia, Salvador, BA, Brazil
| | - D Santana Neta
- Faculty of Medicine, Federal University of Bahia, Salvador, BA, Brazil
| | - G B Carvalho
- Center for Biotechnology and Cell Therapy, Salvador, BA, Brazil
| | - D N Silva
- Center for Biotechnology and Cell Therapy, Salvador, BA, Brazil
| | - B D Paredes
- Center for Biotechnology and Cell Therapy, Salvador, BA, Brazil
| | | | - L A R Freitas
- Faculty of Medicine, Federal University of Bahia, Salvador, BA, Brazil; Gonçalo Moniz Institute, Oswaldo Cruz Foundation (FIOCRUZ), Salvador, BA, Brazil
| | - R D Couto
- Faculty of Pharmacy, Federal University of Bahia, Salvador, BA, Brazil
| | - R R Santos
- Center for Biotechnology and Cell Therapy, Salvador, BA, Brazil; National Institute of Science and Technology for Regenerative Medicine, Rio de Janeiro, RJ, Brazil
| | - B S F Souza
- Center for Biotechnology and Cell Therapy, Salvador, BA, Brazil; Gonçalo Moniz Institute, Oswaldo Cruz Foundation (FIOCRUZ), Salvador, BA, Brazil; National Institute of Science and Technology for Regenerative Medicine, Rio de Janeiro, RJ, Brazil
| | - M B P Soares
- Center for Biotechnology and Cell Therapy, Salvador, BA, Brazil; Gonçalo Moniz Institute, Oswaldo Cruz Foundation (FIOCRUZ), Salvador, BA, Brazil; National Institute of Science and Technology for Regenerative Medicine, Rio de Janeiro, RJ, Brazil
| | - S G Macambira
- Center for Biotechnology and Cell Therapy, Salvador, BA, Brazil; Gonçalo Moniz Institute, Oswaldo Cruz Foundation (FIOCRUZ), Salvador, BA, Brazil; National Institute of Science and Technology for Regenerative Medicine, Rio de Janeiro, RJ, Brazil; Department of Biochemistry and Biophysics, Institute of Health Sciences, Federal University of Bahia, Salvador, BA, Brazil.
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Le Roy T, Llopis M, Lepage P, Bruneau A, Rabot S, Bevilacqua C, Martin P, Philippe C, Walker F, Bado A, Perlemuter G, Cassard-Doulcier AM, Gérard P. Intestinal microbiota determines development of non-alcoholic fatty liver disease in mice. Gut 2013. [PMID: 23197411 DOI: 10.1136/gutjnl-2012-303816] [Citation(s) in RCA: 681] [Impact Index Per Article: 56.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
OBJECTIVE Non-alcoholic fatty liver disease (NAFLD) is prevalent among obese people and is considered the hepatic manifestation of metabolic syndrome. However, not all obese individuals develop NAFLD. Our objective was to demonstrate the role of the gut microbiota in NAFLD development using transplantation experiments in mice. DESIGN Two donor C57BL/6J mice were selected on the basis of their responses to a high-fat diet (HFD). Although both mice displayed similar body weight gain, one mouse, called the 'responder', developed hyperglycaemia and had a high plasma concentration of pro-inflammatory cytokines. The other, called a 'non-responder', was normoglycaemic and had a lower level of systemic inflammation. Germ-free mice were colonised with intestinal microbiota from either the responder or the non-responder and then fed the same HFD. RESULTS Mice that received microbiota from different donors developed comparable obesity on the HFD. The responder-receiver (RR) group developed fasting hyperglycaemia and insulinaemia, whereas the non-responder-receiver (NRR) group remained normoglycaemic. In contrast to NRR mice, RR mice developed hepatic macrovesicular steatosis, which was confirmed by a higher liver concentration of triglycerides and increased expression of genes involved in de-novo lipogenesis. Pyrosequencing of the 16S ribosomal RNA genes revealed that RR and NRR mice had distinct gut microbiota including differences at the phylum, genera and species levels. CONCLUSIONS Differences in microbiota composition can determine response to a HFD in mice. These results further demonstrate that the gut microbiota contributes to the development of NAFLD independently of obesity.
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Joo JI, Yun JW. Gene expression profiling of adipose tissues in obesity susceptible and resistant rats under a high fat diet. Cell Physiol Biochem 2011; 27:327-40. [PMID: 21471722 DOI: 10.1159/000327959] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 02/10/2011] [Indexed: 11/19/2022] Open
Abstract
Different responses to a high fat diet (HFD) can occur even within a group of animals with the same genetic background, such as obesity-prone (OP) or obesity-resistant (OR) phenotypes, on the same feeding. To explain these phenotypes, we performed an analysis of gene expression differences in brown (BAT) and white adipose tissue (WAT) of OP and OR rats. Microarray analysis of transcripts revealed that 91 and 53 genes showed significant differences in expression between the BAT and WAT gene, respectively. Surprisingly, a majority of these genes were significantly down-regulated in adipose tissues in response to HFD feeding. K-means clustering of the expression levels of these genes identified 4 distinct groupings of genes with significant expression levels. Only a limited number of genes were significantly regulated in adipose tissues in response to HFD feeding, whereas expression levels of a large number of genes differed significantly between OP and OR rat. Our observations support that distinct discrepancies exist in gene-expression regulations in adipose tissues, and that alteration likely resulted from significant differences in genes encoding metabolic enzymes. To the best of our knowledge, this study provided the first direct comparison of gene-expression changes between OP and OR rats.
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Affiliation(s)
- Jeong In Joo
- Department of Biotechnology, Daegu University, Kyungsan, Korea
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Proteomic analysis of liver proteins in rats fed with a high-fat diet in response to capsaicin treatments. BIOTECHNOL BIOPROC E 2010. [DOI: 10.1007/s12257-010-0029-8] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/19/2022]
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Li H, Xie Z, Lin J, Song H, Wang Q, Wang K, Su M, Qiu Y, Zhao T, Song K, Wang X, Zhou M, Liu P, Zhao G, Zhang Q, Jia W. Transcriptomic and Metabonomic Profiling of Obesity-Prone and Obesity-Resistant Rats under High Fat Diet. J Proteome Res 2008; 7:4775-83. [DOI: 10.1021/pr800352k] [Citation(s) in RCA: 75] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]
Affiliation(s)
- Houkai Li
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Zuoquan Xie
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Jingchao Lin
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Huaiguang Song
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Qi Wang
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Ke Wang
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Mingming Su
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Yunping Qiu
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Tie Zhao
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Kai Song
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Xiaoyan Wang
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Mingmei Zhou
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Ping Liu
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Guoping Zhao
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Qinghua Zhang
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
| | - Wei Jia
- School of Pharmacy and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, PRC, State Key Laboratory of Medical Genomics and Shanghai Institute of Hematology Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PRC, National Engineering Center for Biochip at Shanghai, 201203, PRC, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, PRC, and Department of Nutrition, University of North Carolina at Greensboro, North
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12
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Nascimento AF, Sugizaki MM, Leopoldo AS, Lima-Leopoldo AP, Luvizotto RAM, Nogueira CR, Cicogna AC. A Hypercaloric pellet-diet cycle induces obesity and co-morbidities in wistar rats. ACTA ACUST UNITED AC 2008; 52:968-74. [DOI: 10.1590/s0004-27302008000600007] [Citation(s) in RCA: 68] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/04/2008] [Accepted: 07/04/2008] [Indexed: 11/22/2022]
Abstract
The present study was carried to develop and analyze the consequences of hypercaloric pellet-diet cycle that promotes obesity in rats. Male Wistar rats were randomly distributed into two groups that received either normal diet (ND; n =32; 3,5 Kcal/g) or a hypercaloric diet (HD; n =32; 4,6 Kcal/g). The ND group received commercial Labina rat feeding while the HD animals received a cycle of five hypercaloric diets over a 14-week period. The effects of the diets were analyzed in terms of body weight, body composition, hormone-metabolite levels, systolic arterial pressure and glucose tolerance at the 5% significance level. The hypercaloric pellet diet cycle promoted an increase in body weight and fat, systolic arterial pressure and a high serum level of glucose, triacylglycerol, insulin and leptin. The HD group also presented an impaired glucose tolerance. In conclusion, the results of this study show that the hypercaloric pellet-diet cycle promoted obesity in Wistar rats and displayed several characteristics that are commonly associated with human obesity, such as high arterial pressure, insulin resistance, hyperglycaemia, hyperinsulinaemia, hyperleptinaemia and dyslipidaemia.
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13
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Influence of increased adiposity on mitochondrial-associated proteins of the rat colon: a proteomic and transcriptomic analysis. Biochim Biophys Acta Mol Basis Dis 2008; 1782:532-41. [PMID: 18598761 DOI: 10.1016/j.bbadis.2008.06.002] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/15/2008] [Revised: 06/04/2008] [Accepted: 06/06/2008] [Indexed: 12/11/2022]
Abstract
Epidemiological studies report obesity to be an important risk factor influencing colon pathologies, yet mechanism(s) are unknown. Recent studies have shown significant elevation of insulin, leptin and triglycerides associated with increased adipose tissue. In situ hybridisation studies have located insulin, leptin and adiponectin receptor expression in the colon epithelia. The influence of increased adiposity and associated deregulation of insulin and adipokines on regulation of the colon epithelium is unknown. Altered adipokine and insulin signalling associated with obesity has an impact on mitochondrial function and mitochondrial dysfunction is increasingly recognised as a contributing factor in many diseases. Proteomics and transcriptomics are potentially powerful methods useful in elucidating the mechanisms whereby obesity increases risk of colon diseases as observed epidemiologically. This study investigated colon mitochondrial-associated protein profiles and corresponding gene expression in colon in response to increased adiposity in a rat model of diet induced obesity. Increased adiposity in diet-induced obese sensitive rats was found to be associated with altered protein expression of 69 mitochondrial-associated proteins involved in processes associated with calcium binding, protein folding, energy metabolism, electron transport chain, structural proteins, protein synthesis and degradation, redox regulation, and transport. The changes in these mitochondrial protein profiles were not correlated with changes at the gene expression level assessed using real-time PCR arrays.
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14
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Noland RC, Thyfault JP, Henes ST, Whitfield BR, Woodlief TL, Evans JR, Lust JA, Britton SL, Koch LG, Dudek RW, Dohm GL, Cortright RN, Lust RM. Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance. Am J Physiol Endocrinol Metab 2007; 293:E31-41. [PMID: 17341547 DOI: 10.1152/ajpendo.00500.2006] [Citation(s) in RCA: 113] [Impact Index Per Article: 6.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
Elevated oxidative capacity, such as occurs via endurance exercise training, is believed to protect against the development of obesity and diabetes. Rats bred both for low (LCR)- and high (HCR)-capacity endurance running provide a genetic model with inherent differences in aerobic capacity that allows for the testing of this supposition without the confounding effects of a training stimulus. The purpose of this investigation was to determine the effects of a high-fat diet (HFD) on weight gain patterns, insulin sensitivity, and fatty acid oxidative capacity in LCR and HCR male rats in the untrained state. Results indicate chow-fed LCR rats were heavier, hypertriglyceridemic, less insulin sensitive, and had lower skeletal muscle oxidative capacity compared with HCR rats. Upon exposure to an HFD, LCR rats gained more weight and fat mass, and their insulin resistant condition was exacerbated, despite consuming similar amounts of metabolizable energy as chow-fed controls. These metabolic variables remained unaltered in HCR rats. The HFD increased skeletal muscle oxidative capacity similarly in both strains, whereas hepatic oxidative capacity was diminished only in LCR rats. These results suggest that LCR rats are predisposed to obesity and that expansion of skeletal muscle oxidative capacity does not prevent excess weight gain or the exacerbation of insulin resistance on an HFD. Elevated basal skeletal muscle oxidative capacity and the ability to preserve liver oxidative capacity may protect HCR rats from HFD-induced obesity and insulin resistance.
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Affiliation(s)
- Robert C Noland
- Department of Physiology, East Carolina University, Greenville, North Carolina 27834, USA
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15
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Li H, Ni Y, Su M, Qiu Y, Zhou M, Qiu M, Zhao A, Zhao L, Jia W. Pharmacometabonomic Phenotyping Reveals Different Responses to Xenobiotic Intervention in Rats. J Proteome Res 2007; 6:1364-70. [PMID: 17311441 DOI: 10.1021/pr060513q] [Citation(s) in RCA: 73] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Abstract
In conventional pharmacological studies, intersubject differences within an animal strain are normally neglected, leading to variations in pharmacological outcomes in response to the same stimulus. Using two classical experimental models, the Streptozotocin (STZ)-induced diabetic model of Wistar rats and the high-energy, diet-induced obesity model of Sprague-Dawley rats, we demonstrate that the different outcomes of STZ or diet intervention are closely associated with variation in predose (baseline) urinary metabolic profiles of the rats. The pharmacometabonomic analysis of predose metabolic profiles indicates that the intersubject difference is, to a great extent, associated with gut-microbiota, which predisposes different pathophysiological outcomes upon diet alteration or chemical stimulus. We hypothesize that there may exist an important association between observations from these two models and the obese/diabetic human population in that subtle variations in metabolic phenotype may predetermine different systems' responses to xenobiotic perturbation, ultimately leading to varied pathophysiological processes. Results from two independent models also suggest that the pharmacometabonomics approach is of great importance in the study of pharmacology and clinical drug evaluations, where endogenous metabolite signatures of predose individuals should be taken into consideration to minimize intersubject difference and the resulting variation in the postdose pharmacological outcomes.
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Affiliation(s)
- Houkai Li
- Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, PRC
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16
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Ricci E, Smallwood S, Chouabe C, Mertani HC, Raccurt M, Morel G, Bonvallet R. Electrophysiological characterization of left ventricular myocytes from obese Sprague-Dawley rat. Obesity (Silver Spring) 2006; 14:778-86. [PMID: 16855186 DOI: 10.1038/oby.2006.90] [Citation(s) in RCA: 27] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
OBJECTIVE Obesity is a complex multifactorial disease that is often associated with cardiac arrhythmias. Various animal models have been used extensively to study the effects of obesity on physiological functions, but, to our knowledge, no study related to ionic membrane currents has been performed on isolated cardiac myocytes. Therefore, we examined the electrophysiological characteristics of four ionic currents from isolated left ventricular myocytes of a high-energy (HE)-induced obesity rat model. RESEARCH METHODS AND PROCEDURES Male Sprague-Dawley rats were fed with either a control diet or a diet containing 33% kcal as fat (HE) for 14 weeks starting at 6 weeks of age. Voltage-clamp experiments were performed on ventricular myocytes. Leptin receptor (ObR) expression was measured using ObR enzyme-linked immunosorbent assay. RESULTS In the HE group, rats designated as obese did not develop a cardiac hypertrophy, either at the organ level or at the cellular level. Densities and kinetics of the L-type calcium current, the transient outward potassium current, the delayed rectifier potassium current, and the sodium-calcium exchange current (I(NCX)) were not significantly different between control and obese rats. A down-regulation of ObR expression was evidenced in the heart of obese rats compared with controls. Acute exposure (5 minutes) of leptin (100 nM) did not induce a significant modification in the current densities either in control or in obese rats, except for I(NCX) density measured in control rats. DISCUSSION The absence of effect of leptin on I(NCX) in obese rats could be a potential arrhythmogenic substrate in obesity.
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Affiliation(s)
- Estelle Ricci
- Unité Mixte de Recherche Centre National de la Recherche Scientifique 5123, Physiologie Intégrative, Cellulaire et Moléculaire, Université Lyon I, Campus La Doua, 69622 Villeurbanne, France
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17
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Pérez-Echarri N, Pérez-Matute P, Martínez JA, Marti A, Moreno-Aliaga MJ. Serum and gene expression levels of leptin and adiponectin in rats susceptible or resistant to diet-induced obesity. J Physiol Biochem 2005; 61:333-42. [PMID: 16180331 DOI: 10.1007/bf03167050] [Citation(s) in RCA: 28] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/22/2022]
Abstract
The aim of the present study was to identify the role of leptin and adiponectin in the development of resistance or susceptibility to diet-induced obesity in rats. For this purpose, male Wistar rats were fed with standard laboratory diet (control group) or cafeteria diet. After 15 days, two groups of rats with different response respect to the cafeteria diet were identified, and were assigned as diet-induced obesity (DIO) and diet resistant (DR) rats. The high-fat diet induced a very significant increase in both body and fat mass weight in DIO group. However, DR rats, gained even less weight than control-fed animals. Food intake was increased in cafeteria-fed rats (both DIO and DR) in comparison to control group; but hyperphagia was higher in DIO rats. In addition, feed efficiency (the ratio of weight gained to calories consumed) was significantly decreased in DR as compared to DIO rats. Regarding leptin, a significant increase in both adipose tissue gene expression and serum levels was observed in DIO rats in comparison with other groups (control and DR). A significant increase in both adiponectin circulating levels and adipose tissue mRNA expression was also observed in DIO animals as compared with the other groups. These data suggest that the susceptibility to obesity of DIO rats might be secondary, at least in part, to an earlier development of leptin resistance, which could lead to alterations in food intake (hyperphagia) and energetic metabolism. However, neither changes in leptin or adiponectin seem to be involved in the adaptive mechanisms that confer resistance to high fat intake.
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Affiliation(s)
- N Pérez-Echarri
- Department of Physiology and Nutrition, University of Navarra, 31008 Pamplona, Spain
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Wang JF, Guo YX, Niu JZ, Liu J, Wang LQ, Li PH. Effects of Radix Puerariae flavones on liver lipid metabolism in ovariectomized rats. World J Gastroenterol 2004; 10:1967-70. [PMID: 15222048 PMCID: PMC4572242 DOI: 10.3748/wjg.v10.i13.1967] [Citation(s) in RCA: 31] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/15/2022] Open
Abstract
AIM: To study the effects of Radix Puerariae flavones (RPF) on liver lipid metabolism in ovariectomized (OVX) rats.
METHODS: Forty adult female Wistar rats were randomly divided into four groups: OVX group; sham-OVX group; OVX + estrogen group and OVX + RPF group. One week after operation rats of the first two groups were treated with physiological saline, rats of OVX + estrogen group with estrogen (1 mg/kg·b.w.) and rats of OVX + RPF group with RPF (100 mg/kg·b.w.), respectively for 5 weeks. After the rats were killed, their body weight, the weight of the abdominal fat and uterus were measured, and the levels of total cholesterol (TC) and triglyceride (TG) in liver homogenate were determined.
RESULTS: Compared with the sham-OVX group, the body mass of the rats in OVX group was found increased significantly; more abdominal fat in store; TC and TG in liver increased and uterine became further atrophy. As a result, the RPF was found to have an inhibitive action on those changes of various degrees.
CONCLUSION: RPF has estrogen-like effect on lipid metabolism in liver and adipose tissue.
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Affiliation(s)
- Ji-Feng Wang
- Department of Biochemistry, Beijing University of Chinese Medicine, Beijing 100029, China
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