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Diets containing soy or rice protein isolate (SPI, RPI) increase insulin sensitivity and improve lipid homeostasis in weanling rats fed high fat, high cholesterol Western diets as a result of activation of PPAR and LXR‐mediated pathways
Author(s) -
Ronis Martin J,
Chen Ying,
Badeaux Jamie,
Shankar Kartik,
Badger Thomas M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.892.2
Subject(s) - medicine , triglyceride , endocrinology , insulin resistance , weanling , cholesterol , glucose homeostasis , cholesterol 7 alpha hydroxylase , liver x receptor , biology , insulin , chemistry , biochemistry , transcription factor , nuclear receptor , gene
Male Sprague‐Dawley rats were placed on AIN‐93G diets containing casein (CAS)on PND24 or onto CAS, SPI or RPI‐based Western diets (Harlan Teklad TD88137) made with high fat and 0.5% cholesterol. Prior to sacrifice on PND50, an oral glucose tolerance test was performed. High fat/high cholesterol feeding impaired glucose disposal (p < 0.05), suggesting peripheral insulin resistance. This was prevented by feeding SPI‐ or RPI‐containing diets (p < 0.05). Increased serum and hepatic triglyceride and cholesterol levels occurred with high fat/cholesterol feeding. Both SPI and RPI reduced serum and hepatic cholesterol (p < 0.05) and hepatic triglyceride levels (p < 0.05). Expression of hepatic PPAR alpha‐, PPAR gamma‐ and LXR‐regulated genes were induced (p < 0.05) by feeding SPI‐ and RPI‐containing diets relative those in CAS‐fed rats, as determined by real time RT‐PCR. This was accompanied by increased binding of the PPARs and LXR to their response elements on the ACO, glucokinase and CYP7A1 gene promoters as measured in EMSA and ChIP assays. Increased expression of PPARs and LXR mRNA and protein were observed (p < 0.05). These data suggest that SPI and RPI elevated insulin sensitivity via increased PPAR gamma signaling, and improved lipid homeostasis as a result of signaling via PPAR alpha and LXR. Supported in part by ARS CRIS #6251‐51000‐005‐00D and the Solae Company (St. Louis, MO).