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As harmful as osteoporosis but less well known - New research better explains sarcopenia

self-reported difficulty with mobility tasks, thus suggesting a role of IGF-I in the causal pathway leading to disability in the elderly. Additional research conducted demonstrated that IL-6 inhibits the secretion of IGF-I and its biological activity and that IL-6 overproduction is a mechanism implicated in IGF-I and insulin-like growth factor-binding protein (IGFBP)-3 downregulation. Furthermore, in transgenic mice, an IGF-I deficiency caused by IL-6-related mechanisms determined growth impairment.

A New Study
In light of such evidence, a potential effect of IL-6 and IGF-I in the regulation of the homeostatic mechanisms that maintain an adequate muscle mass can be claimed. One hypothesis is that IL-6-affected IGF-I production may be a potential mechanism by which chronic inflammation causes impaired physical function.

Italian researchers joined a physiologist from the National Institute of Aging in evaluating the relationship of plasma concentrations of IGF-I and IL-6 with muscle function in a population-based sample of older persons. The authors of "Chronic Inflammation and the Effect of IGF-I on Muscle Strength and Power in Older Persons" are Michelangela Barbieri, Emilia Ragno, and Giuseppe Paolisso, from the Department of Geriatric Medicine and Metabolic Diseases, II University of Naples, Naples; Luigi Ferrucci, Annamaria Corsi, and Stefania Bandinelli, at the Laboratory of Clinical Epidemiology, Italian National Research Council of Aging, Geriatric Department, Florence; Massimiliano Bonafe and Claudio Franceschi, from the Department of Experimental Pathology, University of Bologna, Bologna; Fabiola Olivieri and Simona Giovagnetti, from Italian National Research Centers on Aging, Ancona, all in Italy; and Jack M. Guralnik, at the Epidemiology, Demography, and Biometry Laboratory, National Institute of Aging, Bethesda, MD. Their findings appear in the March 2003 edition American Journal of Physiology--Endocrinology and Metabolism, one o
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
2-Apr-2003


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