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Articles in PresS, published online ahead of print November 5, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00319.2002
Submitted on July 16, 2002
Accepted on October 29, 2002
1 Department of Geriatric Medicine and Metabolic Diseases, II University of Naples, Napoli, Italy
2 Geriatric Department, Italian National Research Center on Aging, Laboratory of Clinical Epidemiology, Florence, Italy
3 Department of Experimental Pathology, University of Bologna, Bologna, Italy
4 Molecolar Biology Section, Italian National Research Center on Aging, Ancona, Italy
5 Epidemiology, Demography and Biometry Laboratory, National Institute of Aging, Bethesda, USA
* To whom correspondence should be addressed. E-mail: giuseppe.paolisso{at}unina2.it.
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 causes a reduction of physical performance in elderly through its effect on muscle function. In vitro studies demonstrated that Interleukin-6 inhibits the secretion of IGF-1 and its biological activity suggesting that the negative effect of Interleukin-6 on muscle function might be mediated through IGF-1. We evaluated the joint effect of IGF-1 and Interleukin-6 on muscle function in a population based sample of 526 persons with a wide age range (20-102 years). After adjusting for potential confounders, such as age, sex, body mass index, IL-6 receptor and IL-6 promoter polymorphism, Interleukin-6, IGF-1, and their interaction were significant predictors of handgrip and muscle power. In analyses stratified by Interleukin-6 tertiles, IGF-1 was an independent predictor of muscle function only in subjects in the lowest Interleukin-6 tertile suggesting that the effect of IGF-1 on muscle function depends on Interleukin-6 levels. This mechanism may explain why Interleukin-6 is a strong risk factor for disability.
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