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1 Longitudinal Studies Section, Clinical Research Branch, National Institute on Aging, Baltimore, Maryland, United States
2 Sanitaria di Firenze, Geriatric Rehabilitation Unit, Florence, Tuscany, Italy
3 Tuscany Region Health Agency, Florence, Tuscany, Italy
* To whom correspondence should be addressed. E-mail: ferruccilu{at}grc.nia.nih.gov.
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" (33). 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 pro-inflammatory 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 years 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 BMI 
30 kg/m2. After adjusting for age, sex, and physical activity, components of sarcopenic obesity were associated with elevated levels of interleukin (IL)-6, C-reactive protein (CRP), IL-1ra, and sIL-6r (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 pro-inflammatory cytokines may be critical in both the development and progression of sarcopenic obesity.
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