Role of growth hormone, insulin-like growth factor-I, and insulin-like growth factor binding proteins in the catabolic response to injury and infection.
The erosion of lean body mass resulting from protracted critical illness remains a significant risk factor for increased morbidity and mortality in this patient population. Previous studies have documented the well known impairment in nitrogen balance results from both an increase in muscle protein degradation as well as a decreased rate of both myofibrillar and sacroplasmic protein synthesis. This protein imbalance may be caused by an increased presence or activity of various catabolic agents, such as tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6 or glucocorticoids, or may be mediated via a decreased concentration or responsiveness to various anabolic hormones, such as growth hormone or insulin-like growth factor-I. This review focuses on recent developments pertaining to the importance of alterations in the growth hormone-insulin-like growth factor-I axis as a mechanism for the observed defects in muscle protein balance.
Lang
Charles H
CH
Department of Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, Pennsylvania 17033, USA. clang@psu.edu
Frost
Robert A
RA
D016638:Critical Illness / Q000628:therapy; D013006:Growth Hormone / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D018969:Insulin-Like Growth Factor Binding Proteins / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000502:physiology*; D009124:Muscle Proteins / Q000378:metabolism*; D055435:Myostatin; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism; D014947:Wounds and Injuries / Q000378:metabolism*
D018969:Insulin-Like Growth Factor Binding Proteins; C525911:MSTN protein, human; D009124:Muscle Proteins; D055435:Myostatin; D016212:Transforming Growth Factor beta; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone