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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #211164
Title: Dietary soy protein isolate attenuates metabolic syndrome in rats via effects on PPAR, LXR and SREBP signaling

Author
item RONIS, MARTIN - Arkansas Children'S Nutrition Research Center (ACNC)
item CHEN, YING - Arkansas Children'S Nutrition Research Center (ACNC)
item BADEAUX, JAMIE - Arkansas Children'S Nutrition Research Center (ACNC)
item BADGER, THOMAS - Arkansas Children'S Nutrition Research Center (ACNC)

Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/20/2009
Publication Date: 8/1/2009
Citation: Ronis, M.J., Chen, Y., Badeaux, J., Badger, T.M. 2009. Dietary soy protein isolate attenuates metabolic syndrome in rats via effects on PPAR, LXR and SREBP signaling. Journal of Nutrition. 139(8):1431-1438.

Interpretive Summary: Body composition (especially percent fat) appears to be influenced by consumption of soy protein isolate (SPI), a partially purified form of soy protein used in infant formula and as an ingredient in many prepared foods. For example, rats fed a standard rodent diet that includes SPI have lower body fat than those fed the same diet made with the milk protein casein. This study investigated the effects of SPI and the phytochemicals bound to SPI (isoflavones) on proteins that regulate genes responsible to fatty acid, glucose, and cholesterol metabolism and transport. We found that soy consumption clearly altered metabolism, but not in a manner that would be expected to result in lower body fat.

Technical Abstract: Male and female rats (age 21 days) were fed AIN-93G diets made with casein, soy protein isolate (SPI+), isoflavone reduced SPI+ (SPI-), or casein plus purified genistein or daidzein. After 2 weeks, peroxisome proliferator activated receptor (PPAR) alpha-regulated genes involved in fatty acid degradation were up-regulated by SPI+ (P < 0.05), accompanied by increased promoter binding and expression of PPAR alpha gamma mRNA (P < 0.05). Feeding SPI- or pure isoflavones did not alter PPAR alpha-regulated gene expression. Similar effects of SPI+ feeding were observed on PPAR gamma signaling. In contrast, SPI+, SPI-, and casein plus isoflavones all increased liver X-receptor (LXR) alpha-regulated genes involved in cholesterol homeostasis. Feeding SPI+ increased promoter binding of LXR alpha and expression of the transcription factor mRNA and protein (P< 0.05). In a second experiment, male Sprague-Dawley rats were fed AIN-93G diets made with casein from PND24 to PND64 or were fed high fat Western diets containing 0.5 percent cholesterol made with casein or SPI+. Insulin resistance, steatosis, and hypercholesterolemia in the Western diet-fed rats were partially prevented by SPI+ (P < 0.05). No effects of SPI+ were observed on sterol receptor element binding protein (SREBP)-1c mRNA, but nuclear SREBP-1c protein and mRNA of enzymes involved in fatty acid synthesis were suppressed (P<0.05). This was associated with reduced expression of the serine protease SKl-1/S1P. These data suggest that activation of PPAR- and LXR-, and inhibition of SREBP-1c signaling may contribute to increased insulin sensitivity and improved lipid homeostasis observed in SPI+-fed rats after consumption of diets high in fat and cholesterol.