Research article summary (published 16 May 2006):

Changes in liver PPARalpha mRNA expression in response to two levels of high-safflower-oil diets correlate with changes in adiposity and serum leptin in rats and mice.

Full Abstract

The ligand-dependent transcription factor peroxisome proliferator-activated receptor alpha (PPARalpha) is known to be activated by common fatty acids and to regulate the expression of genes of various lipid oxidation pathways and transport. High-fat diets provide more fatty acids, which presumably could enhance lipid catabolism through up-regulation of PPARalpha signaling. However, high intake of fat could also lead to obesity. To examine PPARalpha signaling in high-fat feeding and obesity, this study examined the hepatic mRNA expression of PPARalpha and some of its target genes in Wistar rats and C57BL/6J mice fed two levels (20% or 30% wt/wt) of high-safflower-oil (SFO; oleic-acid-rich) diets until animals showed significantly higher body weight (13 weeks for rats and 22 weeks for mice) than those of control groups fed a 5% SFO diet. At the end of these respective feeding periods, only the rats fed 30% SFO and the mice fed 20% SFO among the two groups fed high-fat diets showed significantly higher body weight, white adipose tissue weight, serum leptin and mRNA expression of PPARalpha (P<.05) compared to the respective control groups. Despite elevated acyl-CoA (a PPARalpha target gene) protein and activity in both groups fed high-fat diets, the mRNA expression level of most PPARalpha target genes examined correlated mainly to PPARalpha mRNA levels and not to fat intake or liver lipid levels. The observation that the liver PPARalpha mRNA expression in groups fed high-fat diets was significantly higher only in obese animals with elevated serum leptin implied that obesity and associated hyperleptinemia might have a stronger impact than dietary SFO intake per se on PPARalpha-regulated mRNA expression in the liver.

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Author information

Author/s: Hsu, Shan-Ching (SC); Huang, Ching-jang (CJ);

Affiliation: Division of Nutritional Science, Institute of Microbiology and Biochemistry, College of Life Science, National Taiwan University, Taipei 106, Taiwan.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: The Journal of nutritional biochemistry (J Nutr Biochem), published in United States. (Language: eng)

Reference: 2007-Feb; vol 18 (issue 2) : pp 86-96

Dates: Created 2007/01/12; Completed 2007/03/08;

PMID: 16713235, status: MEDLINE (last retrieval date: 12/26/2008)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Acyl-CoA Oxidase - analysis; genetics; metabolism Adipose Tissue - anatomy & histology Adiposity - genetics Alkane 1-Monooxygenase - analysis Animals Body Weight Dietary Fats, Unsaturated - administration & dosage Eating Fatty Acids, Nonesterified - analysis; blood Gene Expression Regulation Leptin - blood Lipids - analysis; blood

Liver - chemistry; enzymology Male Mice Mice, Inbred C57BL Obesity - blood Organ Size PPAR gamma - genetics RNA, Messenger - analysis Rats Rats, Wistar Safflower Oil - administration & dosage Triglycerides - analysis; blood

Associated Chemicals: Dietary Fats, Unsaturated (0) ; Fatty Acids, Nonesterified (0) ; Leptin (0) ; Lipids (0) ; PPAR gamma (0) ; RNA, Messenger (0) ; Triglycerides (0) ; Safflower Oil (8001-23-8) ; Alkane 1-Monooxygenase (EC 1.14.15.3) ; Acyl-CoA Oxidase (EC 1.3.3.6)

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