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肌醇抑制肠道葡萄糖吸收并促进肌肉葡萄糖摄取:一项双途径研究。

Myo-inositol inhibits intestinal glucose absorption and promotes muscle glucose uptake: a dual approach study.

作者信息

Chukwuma Chika Ifeanyi, Ibrahim Mohammed Auwal, Islam Md Shahidul

机构信息

Department of Biochemistry, School of Life Sciences, University of KwaZulu-Natal (Westville Campus), Durban, 4000, South Africa.

Department of Biochemistry, Ahmadu Bello University, Zaria, Nigeria.

出版信息

J Physiol Biochem. 2016 Dec;72(4):791-801. doi: 10.1007/s13105-016-0517-1. Epub 2016 Sep 6.

DOI:10.1007/s13105-016-0517-1
PMID:27601253
Abstract

The present study investigated the effects of myo-inositol on muscle glucose uptake and intestinal glucose absorption ex vivo as well as in normal and type 2 diabetes model of rats. In ex vivo study, both intestinal glucose absorption and muscle glucose uptake were studied in isolated rat jejunum and psoas muscle respectively in the presence of increasing concentrations (2.5 % to 20 %) of myo-inositol. In the in vivo study, the effect of a single bolus dose (1 g/kg bw) of oral myo-inositol on intestinal glucose absorption, blood glucose, gastric emptying and digesta transit was investigated in normal and type 2 diabetic rats after 1 h of co-administration with 2 g/kg bw glucose, when phenol red was used as a recovery marker. Myo-inositol inhibited intestinal glucose absorption (IC = 28.23 ± 6.01 %) and increased muscle glucose uptake, with (GU = 2.68 ± 0.75 %) or without (GU = 8.61 ± 0.55 %) insulin. Additionally, oral myo-inositol not only inhibited duodenal glucose absorption and reduced blood glucose increase, but also delayed gastric emptying and accelerated digesta transit in both normal and diabetic animals. Results of this study suggest that dietary myo-inositol inhibits intestinal glucose absorption both in ex vivo and in normal or diabetic rats and also promotes muscle glucose uptake in ex vivo condition. Hence, myo-inositol may be further investigated as a possible anti-hyperglycaemic dietary supplement for diabetic foods and food products.

摘要

本研究调查了肌醇对离体以及正常和2型糖尿病大鼠模型的肌肉葡萄糖摄取和肠道葡萄糖吸收的影响。在离体研究中,分别在存在浓度递增(2.5%至20%)的肌醇的情况下,对分离的大鼠空肠和腰大肌的肠道葡萄糖吸收和肌肉葡萄糖摄取进行了研究。在体内研究中,当使用酚红作为回收标记物时,在与2 g/kg体重的葡萄糖共同给药1小时后,研究了单次口服大剂量(1 g/kg体重)肌醇对正常和2型糖尿病大鼠的肠道葡萄糖吸收、血糖、胃排空和消化物转运的影响。肌醇抑制肠道葡萄糖吸收(IC = 28.23 ± 6.01%),并增加肌肉葡萄糖摄取,无论有无胰岛素(有胰岛素时GU = 2.68 ± 0.75%;无胰岛素时GU = 8.61 ± 0.55%)。此外,口服肌醇不仅抑制十二指肠葡萄糖吸收并减少血糖升高,而且在正常和糖尿病动物中均延迟胃排空并加速消化物转运。本研究结果表明,膳食肌醇在离体以及正常或糖尿病大鼠中均抑制肠道葡萄糖吸收,并且在离体条件下还促进肌肉葡萄糖摄取。因此,肌醇可作为糖尿病食品和食品产品中一种可能的抗高血糖膳食补充剂作进一步研究。

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