Ronenn Roubenoff1. 1. Department of Molecular Medicine, Millennium Pharmaceuticals Inc, Cambridge, Massachusetts 02139, USA. roubenoff@mpi.com
Abstract
PURPOSE OF REVIEW: Research in the field of sarcopenia is evolving rapidly, and the process is now recognized as an important cause of frailty and morbidity in the elderly. This review focuses on recent developments in the field, especially regarding the role of catabolic stimuli in causing sarcopenia. RECENT FINDINGS: There is now an impressive body of literature implicating increased interleukin-6 levels in successfully aging adults. New data indicate that high interleukin-6 levels carry a poor prognosis, although it is not clear if the cytokine has primarily a causal or counter-regulatory function. Interleukin-6 and other cytokines could function through direct catabolic effects, or by causing reduced dietary energy intake (the anorexia of aging), or by inducing insulin resistance or lowering growth hormone-insulin-like growth factor-I concentrations. Furthermore, apoptosis has now been linked to sarcopenia, suggesting that an inflammatory signal could trigger loss of muscle cells in the elderly even in the absence of overt inflammatory disease. SUMMARY: Aging causes loss of many of the anabolic signals to muscle that are present in young adulthood. Recent research suggests that there is also an increase in catabolic signals with age.
PURPOSE OF REVIEW: Research in the field of sarcopenia is evolving rapidly, and the process is now recognized as an important cause of frailty and morbidity in the elderly. This review focuses on recent developments in the field, especially regarding the role of catabolic stimuli in causing sarcopenia. RECENT FINDINGS: There is now an impressive body of literature implicating increased interleukin-6 levels in successfully aging adults. New data indicate that high interleukin-6 levels carry a poor prognosis, although it is not clear if the cytokine has primarily a causal or counter-regulatory function. Interleukin-6 and other cytokines could function through direct catabolic effects, or by causing reduced dietary energy intake (the anorexia of aging), or by inducing insulin resistance or lowering growth hormone-insulin-like growth factor-I concentrations. Furthermore, apoptosis has now been linked to sarcopenia, suggesting that an inflammatory signal could trigger loss of muscle cells in the elderly even in the absence of overt inflammatory disease. SUMMARY: Aging causes loss of many of the anabolic signals to muscle that are present in young adulthood. Recent research suggests that there is also an increase in catabolic signals with age.
Authors: Vasant Hirani; Robert G Cumming; Fiona Blyth; Vasi Naganathan; David G Le Couteur; Louise M Waite; David J Handelsman; Markus J Seibel Journal: Age (Dordr) Date: 2015-02-04
Authors: Jama L Purser; Maragatha N Kuchibhatla; Marie L Miranda; Dan G Blazer; Harvey J Cohen; Gerda G Fillenbaum Journal: Biomark Med Date: 2008 Impact factor: 2.851
Authors: Fernanda Matos Coelho; F M S Narciso; D M G Oliveira; D S Pereira; A L Teixeira; M M Teixeira; D G Souza; L S M Pereira Journal: Inflamm Res Date: 2009-08-22 Impact factor: 4.575
Authors: Lygia P Lustosa; Fernanda M Coelho; Juscelio P Silva; Daniele S Pereira; Adriana N Parentoni; João M D Dias; Rosangela C Dias; Leani S M Pereira Journal: Trials Date: 2010-07-28 Impact factor: 2.279