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. 2007 Mar;102(3):919-25.
doi: 10.1152/japplphysiol.00627.2006. Epub 2006 Nov 9.

Sarcopenic obesity and inflammation in the InCHIANTI study

Matthew A Schrager  1 , E Jeffrey Metter, Eleanor Simonsick, Alessandro Ble, Stefania Bandinelli, Fulvio Lauretani, Luigi Ferrucci
Affiliations

Sarcopenic obesity and inflammation in the InCHIANTI study

Matthew A Schrager et al. J Appl Physiol (1985). 2007 Mar.

Abstract

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 > or =30 kg/m(2). 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.

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Figures

Fig. 1
Fig. 1
Cross-classification of study participants according to global obesity, central obesity, and muscle strength. Schematic representation is shown of 4 cross-classified groups for men (M) and women (W) based on tertiles of waist circumference (WC) and body mass index (BMI) ≥ 30 kg/m2. Within each of these 4 body composition groups, M and W in the lowest tertile of grip strength were considered sarcopenic. Cutpoints for BMI, WC, and strength are also shown.
Fig. 2
Fig. 2
Adjusted group mean values for inflammatory markers. Back-transformed mean inflammatory marker level values are shown for C-reactive protein (CRP), IL-6, IL-1 receptor antagonist (IL-1ra), soluble IL-6 receptor (sIL-6r), IL-18, and TNF-α across the 8 cross-classified groups (adjusted for group differences in age, sex, education, smoking history, physical activity, and history of comorbid diseases including diabetes mellitus, hypertension, myocardial infarction, stroke, and heart failure).
Fig. 3
Fig. 3
Proposed final structural equation model for the relationships between age, obesity, central obesity, inflammation, and poor muscle strength. Inflammation is represented by a latent variable (ellipse), which expresses the common relationships between the 6 inflammatory markers. Each variable in the model has a series of arrows that reflect the direction of the a priori proposed relationship between the variables. Path coefficients are standardized and represent the change that occurs in the variable at the head of an arrow for each SD change in the variable at the tail of the arrow. The inflammation latent variable is similar to a factor that is derived during confirmatory factor analysis. It represents the shared variance that exists between the 6 inflammatory markers that are included in the model. All the markers contribute to the variable proportionately to their path coefficient.
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