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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转导受损。

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

机构信息

Division of Cardiology, New York-Presbyterian Hospital, Columbia University Medical Center, New York, NY 10032, USA.

出版信息

Clin Sci (Lond). 2010 Aug 17;119(11):465-6. doi: 10.1042/CS20100363.

DOI:10.1042/CS20100363
PMID:20629636
Abstract

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 of Clinical 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.

摘要

心力衰竭(CHF)患者的全身和局部代谢紊乱会导致疾病的进展。导致运动不耐受的骨骼肌代谢、形态和功能受损是 CHF 综合征的特征。这些变化导致葡萄糖和脂质代谢异常以及相关的胰岛素抵抗,从而导致晚期 HF 患者的骨骼肌分解代谢异常和肌肉萎缩的发展。在本期《临床科学》中,托特及其同事证明了 HF 患者骨骼肌蛋白代谢受损,并特别显示了这些患者在经历营养缺乏期后骨骼肌的合成代谢反应受损。

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