| Exercise ameliorates high-fat diet-induced metabolic and vascular dysfunction, and increases adipocyte progenitor cell population in brown adipose tissue. | |
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MedLine Citation:
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PMID: 21368268 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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A high-fat diet (HFD) is associated with adipose inflammation, which contributes to key components of metabolic syndrome, including obesity and insulin resistance. The increased visceral adipose tissue mass associated with obesity is the result of hyperplasia and hypertrophy of adipocytes. To investigate the effects of exercise on HFD-induced metabolic disorders, male C57BL/6 mice were divided into four groups: SED (sedentary)-ND (normal diet), EX (exercise)-ND, SED-HFD, and EX-HFD. Exercise was performed on a motorized treadmill at 15 m/min, 40 min/day, and 5 day/wk for 8 wk. Exercise resulted in a decrease in abdominal fat contents and inflammation, improvements in glucose tolerance and insulin resistance, and enhancement of vascular constriction and relaxation responses. Exercise with or without HFD increased putative brown adipocyte progenitor cells in brown adipose tissue compared with groups with the same diet, with an increase in brown adipocyte-specific gene expression in brown and white adipose tissue. Exercise training enhanced in vitro differentiation of the preadipocytes from brown adipose depots into brown adipocytes and enhanced the expression of uncoupling protein 1. These findings suggest that exercise ameliorates high-fat diet-induced metabolic disorders and vascular dysfunction, and increases adipose progenitor cell population in brown adipose tissue, which might thereby contribute to enhanced functional brown adipose. |
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Authors:
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Xiaohua Xu; Zhekang Ying; Ming Cai; Zhaobin Xu; Yuanjing Li; Silis Y Jiang; Kevin Tzan; Aixia Wang; Sampath Parthasarathy; Guanglong He; Sanjay Rajagopalan; Qinghua Sun |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2011-03-02 |
Journal Detail:
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Title: American journal of physiology. Regulatory, integrative and comparative physiology Volume: 300 ISSN: 1522-1490 ISO Abbreviation: Am. J. Physiol. Regul. Integr. Comp. Physiol. Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-05-04 Completed Date: 2011-06-30 Revised Date: 2012-09-24 |
Medline Journal Info:
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Nlm Unique ID: 100901230 Medline TA: Am J Physiol Regul Integr Comp Physiol Country: United States |
Other Details:
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Languages: eng Pagination: R1115-25 Citation Subset: IM |
Affiliation:
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Division of Environmental Health Sciences, College of Public Health, The Ohio State University, 460 W 12th Ave., Columbus, OH 43210, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adipocytes
/
metabolism,
pathology*,
ultrastructure Adipogenesis* / genetics Adipose Tissue, Brown / metabolism, pathology* Animals Biological Markers / blood Blood Glucose / metabolism Body Weight Dietary Fats / administration & dosage* Energy Metabolism Flow Cytometry Gene Expression Regulation Inflammation Mediators / blood Insulin / blood Insulin Resistance Ion Channels / genetics, metabolism Magnetic Resonance Imaging Male Metabolic Syndrome X / blood, etiology, pathology, physiopathology, prevention & control* Mice Mice, Inbred C57BL Microscopy, Electron, Transmission Mitochondria / metabolism, ultrastructure Mitochondrial Proteins / genetics, metabolism Physical Exertion* RNA, Messenger / metabolism Sedentary Lifestyle* Stem Cells / metabolism, pathology*, ultrastructure Time Factors Triglycerides / blood Vascular Diseases / blood, etiology, pathology, physiopathology, prevention & control* Vasoconstriction Vasodilation |
| Grant Support | |
ID/Acronym/Agency:
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ES015146/ES/NIEHS NIH HHS; ES016588/ES/NIEHS NIH HHS; ES017412/ES/NIEHS NIH HHS; ES018900/ES/NIEHS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers; 0/Blood Glucose; 0/Dietary Fats; 0/Inflammation Mediators; 0/Insulin; 0/Ion Channels; 0/Mitochondrial Proteins; 0/RNA, Messenger; 0/Triglycerides; 0/mitochondrial uncoupling protein |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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