Document Detail

Offspring from mothers fed a 'junk food' diet in pregnancy and lactation exhibit exacerbated adiposity that is more pronounced in females.
MedLine Citation:
PMID:  18467362     Owner:  NLM     Status:  MEDLINE    
We have shown previously that a maternal junk food diet during pregnancy and lactation plays a role in predisposing offspring to obesity. Here we show that rat offspring born to mothers fed the same junk food diet rich in fat, sugar and salt develop exacerbated adiposity accompanied by raised circulating glucose, insulin, triglyceride and/or cholesterol by the end of adolescence (10 weeks postpartum) compared with offspring also given free access to junk food from weaning but whose mothers were exclusively fed a balanced chow diet in pregnancy and lactation. Results also showed that offspring from mothers fed the junk food diet in pregnancy and lactation, and which were then switched to a balanced chow diet from weaning, exhibited increased perirenal fat pad mass relative to body weight and adipocyte hypertrophy compared with offspring which were never exposed to the junk food diet. This study shows that the increased adiposity was more enhanced in female than male offspring and gene expression analyses showed raised insulin-like growth factor-1 (IGF-1), insulin receptor substrate (IRS)-1, vascular endothelial growth factor (VEGF)-A, peroxisome proliferator-activated receptor-gamma (PPARgamma), leptin, adiponectin, adipsin, lipoprotein lipase (LPL), Glut 1, Glut 3, but not Glut 4 mRNA expression in females fed the junk food diet throughout the study compared with females never given access to junk food. Changes in gene expression were not as marked in male offspring with only IRS-1, VEGF-A, Glut 4 and LPL being up-regulated in those fed the junk food diet throughout the study compared with males never given access to junk food. This study therefore shows that a maternal junk food diet promotes adiposity in offspring and the earlier onset of hyperglycemia, hyperinsulinemia and/or hyperlipidemia. Male and female offspring also display a different metabolic, cellular and molecular response to junk-food-diet-induced adiposity.
S A Bayol; B H Simbi; J A Bertrand; N C Stickland
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-05-08
Journal Detail:
Title:  The Journal of physiology     Volume:  586     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2008 Jul 
Date Detail:
Created Date:  2008-07-02     Completed Date:  2008-11-13     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  3219-30     Citation Subset:  IM    
The Royal Veterinary College, Department of Veterinary Basic Sciences, Royal College Street, London NW1 0TU, UK.
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MeSH Terms
Blood Glucose
Cholesterol / blood
Gene Expression Profiling
Insulin / blood
Prenatal Nutritional Physiological Phenomena*
Sex Characteristics*
Transcription, Genetic
Triglycerides / blood
Grant Support
//Wellcome Trust
Reg. No./Substance:
0/Blood Glucose; 0/Triglycerides; 11061-68-0/Insulin; 57-88-5/Cholesterol

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