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Does high dietary protein intake contribute to the increased risk of developing prediabetes and type 2 diabetes?
Applied Physiology, Nutrition, and Metabolism ( IF 2.4 ) Pub Date : 2020-08-05 , DOI: 10.1139/apnm-2020-0396
Oana Ancu 1 , Monika Mickute 2 , Nicola D Guess 3 , Nicholas M Hurren 1 , Nicholas A Burd 4 , Richard W Mackenzie 1
Affiliation  

Applied Physiology, Nutrition, and Metabolism, Ahead of Print.
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. Novelty: Excess amino acids may over-activate mTOR, resulting in desensitisation of IRS-1 and reduced insulin-mediated glucose uptake.


中文翻译:

高膳食蛋白质摄入量是否会增加患前驱糖尿病和 2 型糖尿病的风险?

应用生理学、营养学和代谢,提前出版。
胰岛素抵抗是一种复杂的代谢紊乱,与许多慢性疾病的发展有关。虽然人们普遍认为体重减轻应该是治疗超重和肥胖个体胰岛素抵抗相关疾病的主要方法,但研究人员对饮食限制期间的最佳蛋白质摄入量没有达成共识。最近,有人提出血浆支链氨基酸浓度的增加与胰岛素抵抗和 2 型糖尿病的发展有关。尚未充分研究过量氨基酸可用性可能导致胰岛素抵抗的确切机制。然而,已经假设,由于胰岛素受体底物 (IRS) 降解和 Akt-AS160 活性降低,哺乳动物雷帕霉素靶标 (mTOR) 复合物 1 在氨基酸过载的情况下过度活化有助于减少胰岛素刺激的葡萄糖摄取。此外,在体重稳定和体重减轻的情况下,高蛋白饮食对胰岛素敏感性的长期影响需要更多的研究。本综述重点关注高蛋白饮食对胰岛素敏感性的影响,并讨论饮食氨基酸影响胰岛素信号传导的潜在机制。新颖性:过量的氨基酸可能会过度激活 mTOR,导致 IRS-1 脱敏并降低胰岛素介导的葡萄糖摄取。
更新日期:2020-08-05
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