中国菰米对高脂膳食诱导大鼠胰岛素抵抗机制的研究

EFFECT OF CHINESE WILD RICE ON INSULIN RESISTANCE IN RATS INDUCED BY HIGH-FAT/CHOLESTEROL DIETS

目的探讨中国菰米对高脂膳食诱导的胰岛素抵抗大鼠的影响及其作用机制。方法 44只雄性SD大鼠按胰岛素抵抗指数(HOMA-IR)随机分为阴性对照、模型、米面和菰米4组,以对应的饲料连续喂养8 w,测定各组大鼠空腹血糖(FBG)、胰岛素(FINS)以及游离脂肪酸(FFA)水平,并计算HOMA-IR;采用RT-PCR或Western blotting法检测大鼠肝脏组织中蛋白酪氨酸磷酸酶-1B(PTP-1B)和胰岛素受体底物-2(IRS-2)mRNA或蛋白的表达。结果模型组大鼠HOMA-IR值及血清FFA显著高于阴性对照组;米面组与模型组HOMA-IR值及血清FFA无显著性差异;菰米组大鼠血清FBG、FINS和FFA浓度及HOMA-IR值显著低于米面组和模型组。菰米组大鼠肝组织中PTP-1B基因和蛋白的表达均明显低于模型组和米面组,而IRS-2 mRNA的表达明显升高。结论菰米具有降低胰岛素抵抗大鼠血糖、胰岛素及FFA水平,并通过抑制PTP-1B的相对表达,进而促进IRS-2的磷酸化,增强胰岛素信号的转导作用,可改善机体胰岛素的敏感性。

Objective To explore the effect of Chinese wild rice on insulin resistance in rats induced by high-fat/ cholesterol diets.Methods Forty four male 10-week Sprague-Dawlay rats were randomly divided into four groups according to homeostasis model assessment of insulin resistance（HOMA-IR）： control group（NC）,model group（M）,white rice/processed wheat starch group（WP） and wild rice group（WR）.All groups were given different experimental diets for 8 weeks.Serum fasting blood glucose（FBG）,insulin（FINS） and free fatty acid（FFA） were consecutively measured,and HOMA-IR was calculated.Gene or protein expression of protein tyrosine phosphatase 1B（PTP-1B） and insulin receptor substrate-2（IRS-2） in the liver tissue were analyzed by RT-PCR or Western blotting method.Results The insulin resistance model of SD rats was successfully induced.Compared with model group and white rice/processed wheat starch group,the indices including FBG,FINS,HOMA-IR and FFA were significantly decreased in wild rice group.There were no significant differences between model group and white rice/processed wheat starch group in these indices.Gene and protein expression of PTP-1B in wild rice group was significantly lower than that in model group and white rice/processed wheat starch group.However,mRNA level of IRS-2 was much higher than that in the two groups.Conclusion Wild rice could ameliorate glucose metabolism and insulin sensitivity through inhibiting relative level of PTP-1B and then promoting IRS-2 level in the liver tissue of rats.