Protein catabolism and impairment of skeletal muscle insulin signalling in heart failure.

Protein catabolism and impairment of skeletal muscle insulin signalling in heart failure.
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心力衰竭中的蛋白质分解代谢和骨骼肌胰岛素信号传导受损。

DOI:
10.1042/cs20100363
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发表时间:
2010
期刊:
Clinical science (London, England : 1979)
影响因子:
--
通讯作者:
Schulze,PChristian
Schulze,PChristian
中科院分区:
--
文献类型:
--
作者:
Schulze,PChristian

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慢性心力衰竭(CHF)患者会出现全身和局部代谢紊乱,并导致疾病的进展。骨骼肌代谢、形态和功能受损导致运动不耐受是慢性心力衰竭综合征的标志。这些变化导致糖脂代谢异常,以及相关的胰岛素抵抗,从而导致晚期心衰患者骨骼肌分解代谢的进展和肌肉萎缩的发展。在本期的《临床科学》杂志上,Toth和他的同事证明了HF患者骨骼肌蛋白质代谢的损害,特别是在营养缺乏一段时间后,这些患者骨骼肌的合成代谢反应受损。
Derangements in systemic and local metabolism develop in patients with CHF [chronic HF (heart failure)] and contribute to the progression of the disease. Impaired skeletal muscle metabolism, morphology and function leading to exercise intolerance are hallmarks of the syndrome of CHF. These changes result in abnormal glucose and lipid metabolism, and the associated insulin resistance, which contribute to progression of skeletal muscle catabolism and development of muscle atrophy in patients with advanced HF. In the present issue ofClinical Science, Toth and co-workers demonstrate the impairment of skeletal muscle protein metabolism in patients with HF, and specifically show an impaired anabolic response in the skeletal muscle of these patients following a period of nutritional deficiency.
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