Document Detail


Site-specific changes in the expression of fat-partitioning genes in weanling rats exposed to a low-protein diet in utero.
MedLine Citation:
PMID:  12634446     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Intrauterine growth restriction is associated with increased prevalence of the metabolic syndrome in adult life, including increased adiposity. The aim of this study was to investigate if maternal protein energy malnutrition is associated with changes in expression of genes involved in fat partitioning in weanling rats. RESEARCH METHODS AND PROCEDURES: Time-mated mothers were placed on one of two isocaloric diets, low protein [(LP), 8% protein] or control (20% protein). All mothers remained on the diet throughout pregnancy and lactation. A third group received control for 2 weeks and was switched to LP for the last week of pregnancy and lactation [late low protein (LLP) group]. Offspring were analyzed at weaning for serum glucose, nonesterified fatty acids, triglyceride, and insulin. Expression of the genes acetyl-coenzyme A carboxylase, fatty acid synthase, and carnitine palmitoyl transferase 1 were measured in liver, quadriceps muscle, and subcutaneous white adipose tissue using semiquantitative reverse transcription-polymerase chain reaction. RESULTS: LLP and LP offspring were shorter, weighed less, had reduced serum insulin and nonesterified fatty acids, and had increased serum glucose, serum triglycerides, and hepatic triglycerides. Hepatic gene expression of acetyl-coenzyme A carboxylase and fatty acid synthase was increased 2-fold in LLP and LP offspring (p < 0.001). These changes were not seen in muscle or subcutaneous white adipose tissue. CPT-1 gene expression was unaltered in all tissues examined. DISCUSSION: Maternal protein energy malnutrition programs gene expression of lipogenic enzymes in the liver of weanling offspring in a manner favoring fat synthesis that may predispose these offspring to fat accumulation and insulin resistance later in life.
Authors:
Chris A Maloney; Alison K Gosby; Jenny L Phuyal; Gareth S Denyer; Janet M Bryson; Ian D Caterson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Obesity research     Volume:  11     ISSN:  1071-7323     ISO Abbreviation:  Obes. Res.     Publication Date:  2003 Mar 
Date Detail:
Created Date:  2003-03-13     Completed Date:  2003-06-19     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9305691     Medline TA:  Obes Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  461-8     Citation Subset:  IM    
Affiliation:
Human Nutrition Unit, School of Molecular and Microbial Biosciences, University of Sydney, Sydney, New South Wales, Australia. cmaloney@mmb.usyd.edu.au
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MeSH Terms
Descriptor/Qualifier:
Acetyl-CoA Carboxylase / genetics
Adipose Tissue / enzymology
Animals
Blood Glucose / analysis
Body Composition / genetics*
Carnitine O-Palmitoyltransferase / genetics
Diet, Protein-Restricted*
Fatty Acid Synthetase Complex / genetics
Fatty Acids, Nonesterified / blood
Female
Gene Expression*
Insulin / blood
Lactation
Liver / chemistry,  enzymology
Muscle, Skeletal / enzymology
Pregnancy
Prenatal Exposure Delayed Effects*
Protein-Energy Malnutrition / enzymology
Rats
Rats, Wistar
Reverse Transcriptase Polymerase Chain Reaction
Triglycerides / analysis,  blood
Weaning*
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Fatty Acids, Nonesterified; 0/Triglycerides; 11061-68-0/Insulin; EC 2.3.1.21/Carnitine O-Palmitoyltransferase; EC 6.-/Fatty Acid Synthetase Complex; EC 6.4.1.2/Acetyl-CoA Carboxylase

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


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