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J Appl Physiol 102: 919-925, 2007. First published November 9, 2006; doi:10.1152/japplphysiol.00627.2006 Free Article
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Sarcopenic obesity and inflammation in the InCHIANTI study

Matthew A. Schrager,1 E. Jeffrey Metter,1 Eleanor Simonsick,1 Alessandro Ble,1 Stefania Bandinelli,2 Fulvio Lauretani,3 and Luigi Ferrucci1

1Longitudinal Studies Section, Clinical Research Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland; 2Geriatric Rehabilitation Unit, Azienda Sanitaria di Firenze; and 3Tuscany Region Health Agency, Florence, Italy

Submitted 5 June 2006 ; accepted in final form 3 November 2006

The aging process is often paralleled by decreases in muscle and increases in fat mass. At the extreme these two processes lead to a condition known as "sarcopenic obesity" (Roubenoff R. Ann NY Acad Sci 904: 553–557, 2000). Research suggests that inflammatory cytokines produced by adipose tissue, especially visceral fat, accelerate muscle catabolism and thus contribute to the vicious cycle that initiates and sustains sarcopenic obesity. We tested the hypothesis that obesity and poor muscle strength, hallmarks of sarcopenic obesity, are associated with high circulating levels of proinflammatory cytokines in a random sample of the residents of two municipalities in the Chianti geographic area (Tuscany, Italy). The study sample consisted of 378 men and 493 women 65 yr and older with complete data on anthropometrics, handgrip strength, and inflammatory markers. Participants were cross-classified according to sex-specific tertiles of waist circumference and grip strength and according to a cut point for obesity of body mass index ≥30 kg/m2. After adjusting for age, sex, education, smoking history, physical activity, and history of comorbid diseases, components of sarcopenic obesity were associated with elevated levels of IL-6, C-reactive protein, IL-1 receptor antagonist, and soluble IL-6 receptor (P < 0.05). Our findings suggest that global obesity and, to a greater extent, central obesity directly affect inflammation, which in turn negatively affects muscle strength, contributing to the development and progression of sarcopenic obesity. These results suggest that proinflammatory cytokines may be critical in both the development and progression of sarcopenic obesity.

sarcopenia; central obesity; proinflammatory cytokines



Address for reprint requests and other correspondence: L. Ferrucci, National Institute on Aging, Harbor Hospital, 5th Floor, 3001 S. Hanover St., Baltimore, MD 21225 (e-mail: ferruccilu{at}grc.nia.nih.gov)




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