Document Detail


Dietary soy protein isolate attenuates metabolic syndrome in rats via effects on PPAR, LXR, and SREBP signaling.
MedLine Citation:
PMID:  19515742     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To determine the effects of feeding soy or isoflavones on lipid homeostasis in early development, weanling rats were fed AIN-93G diets made with casein, soy protein isolate (SPI+), isoflavone-reduced SPI+ (SPI-), or casein supplemented with genistein or daidzein for 14 d. PPARalpha-regulated genes and proteins involved in fatty acid degradation were upregulated by SPI+ (P < 0.05) accompanied by increased promoter binding and expression of PPARalpha mRNA (P < 0.05). Feeding SPI- or pure isoflavones did not alter PPARalpha-regulated pathways. SPI+ feeding had similar effects on PPARgamma signaling. SPI+, SPI-, and casein plus isoflavones all increased liver X-receptor (LXR)alpha-regulated genes and enzymes involved in cholesterol homeostasis. Feeding SPI+ increased promoter binding of LXRalpha, expression of the transcription factor mRNA, and protein (P < 0.05). In a second experiment, male Sprague-Dawley rats were fed casein diets from postnatal d (PND) 24 to PND64 or were fed high-fat Western diets containing 5 g x kg(-1) cholesterol made with either casein or SPI+. Insulin resistance, steatosis, and hypercholesterolemia in the Western diet-fed rats were partially prevented by SPI+ (P < 0.05). Nuclear sterol receptor element binding protein (SREBP)-1c protein and mRNA and protein expression of enzymes involved in fatty acid synthesis were increased by feeding Western diets containing casein but not SPI+ (P < 0.05). These data suggest that activation of PPAR and LXR signaling and inhibition of SREBP-1c signaling may contribute to insulin sensitization and improved lipid homeostasis in SPI+-fed rats after consumption of diets high in fat and cholesterol.
Authors:
Martin J Ronis; Ying Chen; Jamie Badeaux; Thomas M Badger
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-06-10
Journal Detail:
Title:  The Journal of nutrition     Volume:  139     ISSN:  1541-6100     ISO Abbreviation:  J. Nutr.     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-07-21     Completed Date:  2009-08-13     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0404243     Medline TA:  J Nutr     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1431-8     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72202, USA. ronismartinj@uams.edu <ronismartinj@uams.edu>
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MeSH Terms
Descriptor/Qualifier:
Animals
Anticholesteremic Agents / pharmacology,  therapeutic use
Caseins / administration & dosage,  pharmacology
Cholesterol / metabolism
DNA-Binding Proteins / genetics,  metabolism*
Dietary Fats
Fatty Liver / prevention & control
Female
Gene Expression / drug effects
Genistein / pharmacology,  therapeutic use
Hypercholesterolemia / prevention & control
Insulin Resistance
Isoflavones / pharmacology,  therapeutic use*
Lipid Metabolism / drug effects*
Male
Metabolic Syndrome X / drug therapy,  genetics,  metabolism*
Orphan Nuclear Receptors
PPAR alpha / genetics,  metabolism*
PPAR gamma / metabolism
Promoter Regions, Genetic / drug effects
RNA, Messenger / metabolism
Rats
Rats, Sprague-Dawley
Receptors, Cytoplasmic and Nuclear / genetics,  metabolism*
Signal Transduction / drug effects
Soybean Proteins / pharmacology,  therapeutic use*
Sterol Regulatory Element Binding Protein 1 / metabolism*
Weight Gain / drug effects
Chemical
Reg. No./Substance:
0/Anticholesteremic Agents; 0/Caseins; 0/DNA-Binding Proteins; 0/Dietary Fats; 0/Isoflavones; 0/Orphan Nuclear Receptors; 0/PPAR alpha; 0/PPAR gamma; 0/RNA, Messenger; 0/Receptors, Cytoplasmic and Nuclear; 0/Soybean Proteins; 0/Sterol Regulatory Element Binding Protein 1; 0/liver X receptor; 446-72-0/Genistein; 486-66-8/daidzein; 57-88-5/Cholesterol

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


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