Document Detail


Moderate daily exercise activates metabolic flexibility to prevent prenatally induced obesity.
MedLine Citation:
PMID:  18772230     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Obesity and its associated comorbidities are of major worldwide concern. It is now recognized that there are a number of metabolically distinct pathways of obesity development. The present paper investigates the effect of moderate daily exercise on the underlying mechanisms of one such pathway to obesity, through interrogation of metabolic flexibility. Pregnant Wistar rats were either fed chow ad libitum or undernourished throughout pregnancy, generating control or intrauterine growth restricted (IUGR) offspring, respectively. At 250 d of age, dual-emission x-ray absorptiometry scans and plasma analyses showed that moderate daily exercise, in the form of a measured amount of wheel running (56 m/d), prevented the development of obesity consistently observed in nonexercised IUGR offspring. Increased plasma C-peptide and hepatic atypical protein kinase Czeta levels explained increased glucose uptake and increased hepatic glycogen storage in IUGR offspring. Importantly, whereas circulating levels of retinol binding protein 4 were elevated in obese, nonexercised IUGR offspring, indicative of glucose sparing without exercise, retinol binding protein 4 levels were normalized in the exercised IUGR group. These data suggest that IUGR offspring have increased flexibility of energy storage and use and that moderate daily exercise prevents obesity development through activation of distinct pathways of energy use. Thus, despite a predisposition to develop obesity under sedentary conditions, obesity development was prevented in IUGR offspring when exercise was available. These results emphasize the importance of tailored lifestyle changes that activate distinct pathways of metabolic flexibility for obesity prevention.
Authors:
Jennifer L Miles; Korinna Huber; Nichola M Thompson; Michael Davison; Bernhard H Breier
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-09-04
Journal Detail:
Title:  Endocrinology     Volume:  150     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2008-12-30     Completed Date:  2009-03-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  179-86     Citation Subset:  AIM; IM    
Affiliation:
Liggins Institute, Faculty of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand.
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MeSH Terms
Descriptor/Qualifier:
Animal Feed
Animals
Blood Glucose / metabolism
Body Composition
C-Peptide / blood
Diet, Reducing / veterinary
Energy Intake
Female
Fetal Growth Retardation / epidemiology,  etiology
Insulin / blood
Leptin / blood
Lipids / blood
Obesity / embryology*,  prevention & control*
Physical Conditioning, Animal*
Pregnancy
Rats
Rats, Wistar
Retinol-Binding Proteins, Plasma / metabolism
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/C-Peptide; 0/Leptin; 0/Lipids; 0/Rbp4 protein, rat; 0/Retinol-Binding Proteins, Plasma; 11061-68-0/Insulin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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