4.7 Editorial Material

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

期刊

CLINICAL SCIENCE
卷 119, 期 11-12, 页码 465-466

出版社

PORTLAND PRESS LTD
DOI: 10.1042/CS20100363

关键词

amino acid; cachexia; heart failure; inflammation; insulin; proteolysis; sarcopenia

资金

  1. NHLBI NIH HHS [K23 HL095742] Funding Source: Medline

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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.

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