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1 Department of Geriatric Medicine and Metabolic Diseases, II University of Naples, I-80138 Naples; 2 Laboratory of Clinical Epidemiology, Italian National Research Council of Aging Geriatric Department, 50125 Florence; 3 Department of Experimental Pathology, University of Bologna, 40126 Bologna; 4 Italian National Research Centers on Aging, 60100 Ancona, Italy; and 5 Epidemiology, Demography, and Biometry Laboratory, National Institute of Aging, Bethesda, Maryland 20814
Deregulation of the inflammatory response plays a major role in the age-related decline of physical performance. The causal pathway leading from inflammation to disability has not been fully clarified, but several researches suggest that interleukin-6 (IL-6) causes a reduction of physical performance in elderly through its effect on muscle function. In vitro studies demonstrated that IL-6 inhibits the secretion of insulin-like growth factor I (IGF-I) and its biological activity, suggesting that the negative effect of IL-6 on muscle function might be mediated through IGF-I. We evaluated the joint effect of IGF-I and IL-6 on muscle function in a population-based sample of 526 persons with a wide age range (20-102 yr). After adjusting for potential confounders, such as age, sex, body mass index, IL-6 receptor, and IL-6 promoter polymorphism, IL-6, IGF-I, and their interaction were significant predictors of handgrip and muscle power. In analyses stratified by IL-6 tertiles, IGF-I was an independent predictor of muscle function only in subjects in the lowest IL-6 tertile, suggesting that the effect of IGF-I on muscle function depends on IL-6 levels. This mechanism may explain why IL-6 is a strong risk factor for disability.
muscle function; disability; aging; InCHIANTI Study; insulin-like growth factor I
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