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Biochemical, Molecular, and Genetic Mechanisms

Dietary Soy Protein Isolate Attenuates Metabolic Syndrome in Rats via Effects on PPAR, LXR, and SREBP Signaling^1–3,

⁴ Department of Pharmacology and Toxicology, ⁵ Arkansas Children's Nutrition Center, and ⁶ Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR 72202

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. PPAR-regulated genes and proteins involved in fatty acid degradation were upregulated by SPI+ (P < 0.05) accompanied by increased promoter binding and expression of PPAR mRNA (P < 0.05). Feeding SPI– or pure isoflavones did not alter PPAR-regulated pathways. SPI+ feeding had similar effects on PPAR signaling. SPI+, SPI–, and casein plus isoflavones all increased liver X-receptor (LXR)-regulated genes and enzymes involved in cholesterol homeostasis. Feeding SPI+ increased promoter binding of LXR, 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·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.

^* To whom correspondence should be addressed. E-mail: ronismartinj{at}uams.edu.

Manuscript received 11 March 2009. Initial review completed 25 March 2009. Revision accepted 20 May 2009.

Published online 10 June 2009.