Document Detail


Exercise ameliorates high-fat diet-induced metabolic and vascular dysfunction, and increases adipocyte progenitor cell population in brown adipose tissue.
MedLine Citation:
PMID:  21368268     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-03-02
Journal Detail:
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:
Created Date:  2011-05-04     Completed Date:  2011-06-30     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R1115-25     Citation Subset:  IM    
Affiliation:
Division of Environmental Health Sciences, College of Public Health, The Ohio State University, 460 W 12th Ave., Columbus, OH 43210, USA.
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MeSH Terms
Descriptor/Qualifier:
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:
ES015146/ES/NIEHS NIH HHS; ES016588/ES/NIEHS NIH HHS; ES017412/ES/NIEHS NIH HHS; ES018900/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
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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