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2 型糖尿病中氨基酸和蛋白质代谢的胰岛素抵抗。

Insulin resistance of amino acid and protein metabolism in type 2 diabetes.

机构信息

Dept. of Clinical and Experimental Medicine, Metabolism Division, University of Padova, Italy.

出版信息

Clin Nutr. 2011 Jun;30(3):267-72. doi: 10.1016/j.clnu.2011.02.009. Epub 2011 Apr 13.

Abstract

Although insulin resistance in T2DM (type 2 diabetes mellitus) is usually referred to glucose and lipid metabolism, the question whether such a resistance affects also amino acid and protein metabolism is both relevant and not easy to be answered. Available data indicate a reduced response to insulin in the inhibition of proteolysis at low, near basal hormone levels, whereas such a response appears to be normal at high physiological doses. In most studies in T2DM subjects the stimulation of whole-body protein synthesis in the presence of hyperinsulinemia and euaminoacidemia appears to be normal, although one single study reported lower rates in male T2DM subjects with obesity. The response to insulin of plasma protein synthesis (albumin and fibrinogen) is also normal. However, some metabolic steps of amino acids related to vascular complications (methionine and arginine) exhibit a defective response to insulin in T2DM subjects with nephropathy. In summary, although gross alterations in the response of whole-body protein turnover are not evident in T2DM, specific investigations reveal subtle abnormalities in metabolic steps of selected amino acids. Furthermore, the effects of interaction between diabetes (with the associated insulin resistance) and older age in the pathogenesis of sarcopenia in the elderly deserve more specific studies.

摘要

虽然 2 型糖尿病(T2DM)中的胰岛素抵抗通常涉及葡萄糖和脂质代谢,但这种抵抗是否也会影响氨基酸和蛋白质代谢的问题是相关的,且不容易回答。现有数据表明,在低激素水平(接近基础水平)时,胰岛素对蛋白水解的抑制作用减弱,而在高生理剂量时,这种反应似乎是正常的。在 T2DM 患者的大多数研究中,在高胰岛素血症和正氨基酸血症存在的情况下,全身蛋白质合成的刺激似乎是正常的,尽管有一项研究报告称肥胖的男性 T2DM 患者的合成率较低。胰岛素对血浆蛋白质合成(白蛋白和纤维蛋白原)的刺激也是正常的。然而,与血管并发症相关的一些氨基酸的代谢步骤(蛋氨酸和精氨酸)在有肾病的 T2DM 患者中对胰岛素的反应存在缺陷。总之,虽然 T2DM 患者全身蛋白质周转率的总体变化不明显,但特定的研究揭示了选定氨基酸的代谢步骤存在细微的异常。此外,糖尿病(伴发的胰岛素抵抗)和老年因素在老年人肌少症发病机制中的相互作用的影响值得更具体的研究。

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