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长期摄入大米可提高高脂饮食喂养小鼠的胰岛素敏感性。

Long-term intake of rice improves insulin sensitivity in mice fed a high-fat diet.

作者信息

Choi Won Hee, Um Min Young, Ahn Jiyun, Jung Chang Hwa, Ha Tae Youl

机构信息

Metabolism and Nutrition Research Group, Korea Food Research Institute, Seongnam, Republic of Korea; Division of Food Biotechnology, University of Science and Technology, Daejeon, Republic of Korea.

Metabolism and Nutrition Research Group, Korea Food Research Institute, Seongnam, Republic of Korea.

出版信息

Nutrition. 2014 Jul-Aug;30(7-8):920-7. doi: 10.1016/j.nut.2013.12.021. Epub 2014 Jan 10.

Abstract

OBJECTIVE

The aim of this study was to evaluate the effects of rice as a carbohydrate source and its molecular mechanisms on insulin resistance induced by a high-fat diet (HFD).

METHODS

C57 BL/6 J mice were divided into three groups and were fed a low-fat diet (LFD); a HFD (with 18% fat, 0.5% cholesterol, 51.5% w/w cornstarch and sucrose); or a HFD with rice (HFD-CR, with 18% fat, 0.5% cholesterol and 51.5% w/w rice powder) for 12 wk. In the HFD-CR diet, cooked rice powder was substituted for cornstarch and sucrose in the HFD as a carbohydrate source.

RESULTS

HFD-CR-fed mice had significantly lower body weight, blood glucose, insulin and leptin levels and ameliorated glucose responses with decreased homeostasis model assessment-insulin resistance compared with HFD-fed mice. Hepatic mRNA levels of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase were down-regulated in the HFD-CR group. The hypertrophied islet size and the decreased pancreatic mRNA expression of glucose transporter 2 in the HFD group were normalized with cooked rice consumption. Rice promoted glucose uptake by activating AMP-activated protein kinase and downstream glucose transporter 4 in the skeletal muscle.

CONCLUSION

Rice consumption as a carbohydrate source might potentiate improvements in glucose uptake via AMP-activated protein kinase activation and glucose transporter 4 expression in the skeletal muscles, thereby improving insulin sensitivity.

摘要

目的

本研究旨在评估大米作为碳水化合物来源对高脂饮食(HFD)诱导的胰岛素抵抗的影响及其分子机制。

方法

将C57 BL/6 J小鼠分为三组,分别给予低脂饮食(LFD);高脂饮食(含18%脂肪、0.5%胆固醇、51.5% w/w玉米淀粉和蔗糖);或高脂大米饮食(HFD-CR,含18%脂肪、0.5%胆固醇和51.5% w/w米粉),持续12周。在HFD-CR饮食中,用熟米粉替代HFD中的玉米淀粉和蔗糖作为碳水化合物来源。

结果

与高脂饮食喂养的小鼠相比,高脂大米饮食喂养的小鼠体重、血糖、胰岛素和瘦素水平显著降低,葡萄糖反应改善,稳态模型评估-胰岛素抵抗降低。高脂大米饮食组肝磷酸烯醇式丙酮酸羧激酶和葡萄糖-6-磷酸酶的mRNA水平下调。食用熟大米可使高脂饮食组胰岛肥大的大小和胰腺葡萄糖转运蛋白2 mRNA表达的降低恢复正常。大米通过激活骨骼肌中的AMP活化蛋白激酶和下游葡萄糖转运蛋白4促进葡萄糖摄取。

结论

作为碳水化合物来源食用大米可能通过激活AMP活化蛋白激酶和骨骼肌中葡萄糖转运蛋白-4的表达来增强葡萄糖摄取的改善,从而提高胰岛素敏感性。

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