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高膳食蛋白质摄入量会增加患糖尿病前期和2型糖尿病的风险吗?

Does high dietary protein intake contribute to the increased risk of developing prediabetes and type 2 diabetes?

作者信息

Ancu Oana, Mickute Monika, Guess Nicola D, Hurren Nicholas M, Burd Nicholas A, Mackenzie Richard W

机构信息

Department of Life Sciences, University of Roehampton, London SW15 4DJ, UK.

Diabetes Research Centre, University of Leicester and the NIHR Leicester Biomedical Research Centre, Leicester, LE17RH, UK.

出版信息

Appl Physiol Nutr Metab. 2021 Jan;46(1):1-9. doi: 10.1139/apnm-2020-0396. Epub 2020 Aug 5.

DOI:10.1139/apnm-2020-0396
PMID:32755490
Abstract

Insulin resistance is a complex metabolic disorder implicated in the development of many chronic diseases. While it is generally accepted that body mass loss should be the primary approach for the management of insulin resistance-related disorders in overweight and obese individuals, there is no consensus among researchers regarding optimal protein intake during dietary restriction. Recently, it has been suggested that increased plasma branched-chain amino acids concentrations are associated with the development of insulin resistance and type 2 diabetes. The exact mechanism by which excessive amino acid availability may contribute to insulin resistance has not been fully investigated. However, it has been hypothesised that mammalian target of rapamycin (mTOR) complex 1 hyperactivation in the presence of amino acid overload contributes to reduced insulin-stimulated glucose uptake because of insulin receptor substrate (IRS) degradation and reduced Akt-AS160 activity. In addition, the long-term effects of high-protein diets on insulin sensitivity during both weight-stable and weight-loss conditions require more research. This review focusses on the effects of high-protein diets on insulin sensitivity and discusses the potential mechanisms by which dietary amino acids can affect insulin signalling. Excess amino acids may over-activate mTOR, resulting in desensitisation of IRS-1 and reduced insulin-mediated glucose uptake.

摘要

胰岛素抵抗是一种复杂的代谢紊乱,与许多慢性疾病的发生发展有关。虽然人们普遍认为体重减轻应是超重和肥胖个体管理胰岛素抵抗相关疾病的主要方法,但研究人员对于饮食限制期间的最佳蛋白质摄入量尚未达成共识。最近,有人提出血浆支链氨基酸浓度升高与胰岛素抵抗和2型糖尿病的发生有关。过量氨基酸可用性可能导致胰岛素抵抗的确切机制尚未得到充分研究。然而,据推测,在氨基酸过载的情况下,雷帕霉素靶蛋白(mTOR)复合物1的过度激活会导致胰岛素刺激的葡萄糖摄取减少,这是由于胰岛素受体底物(IRS)降解和Akt-AS160活性降低所致。此外,高蛋白饮食在体重稳定和体重减轻情况下对胰岛素敏感性的长期影响还需要更多研究。本综述重点关注高蛋白饮食对胰岛素敏感性的影响,并讨论膳食氨基酸影响胰岛素信号传导的潜在机制。过量氨基酸可能过度激活mTOR,导致IRS-1脱敏并减少胰岛素介导的葡萄糖摄取。

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