Rice Bran Protein Hydrolysates Improve Insulin Resistance and Decrease Pro-inflammatory Cytokine Gene Expression in Rats Fed a High Carbohydrate-High Fat Diet

Nutrients

Supawan Thawornchinsombut¹  Veerapol Kukongviriyapan²  Patchareewan Pannangpetch²  Bunkerd Kongyingyoes²  Kampeebhorn Boonloh²  Upa Kukongviriyapan³ 

[1] Department of Food technology, Faculty of Technology, Khon Kaen University, Khon Kaen 40002, Thailand;Department of Pharmacology, Faculty of Medicine, Khon Kaen University, 123 Mittraparp Highway, Muang District, Khon Kaen 40002, Thailand;Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand;

关键词: metabolic syndrome;    insulin resistance;    rice bran protein hydrolysates (RBP);    inflammatory cytokines;   

DOI  :  10.3390/nu7085292

来源: DOAJ

【 摘 要 】

A high carbohydrate-high fat (HCHF) diet causes insulin resistance (IR) and metabolic syndrome (MS). Rice bran has been demonstrated to have anti-dyslipidemic and anti-atherogenic properties in an obese mouse model. In the present study, we investigated the beneficial effects of rice bran protein hydrolysates (RBP) in HCHF-induced MS rats. After 12 weeks on this diet, the HCHF-fed group was divided into four subgroups, which were orally administered RBP 100 or 500 mg/kg, pioglitazone 10 mg/kg, or tap water for a further 6 weeks. Compared with normal diet control group, the MS rats had elevated levels of blood glucose, lipid, insulin, and HOMA-IR. Treatment with RBP significantly alleviated all those changes and restored insulin sensitivity. Additionally, RBP treatment increased adiponectin and suppressed leptin levels. Expression of Ppar-γ mRNA in adipose tissues was significantly increased whereas expression of lipogenic genes Srebf1 and Fasn was significantly decreased. Levels of mRNA of proinflammatory cytokines, Il-6, Tnf-α, Nos-2 and Mcp-1 were significantly decreased. In conclusion, the present findings support the consumption of RBP as a functional food to improve insulin resistance and to prevent the development of metabolic syndrome.

【 授权许可】

Unknown