The impact of insulin resistance and inflammation on the association between sarcopenic obesity and physical...

Age associated increases in visceral adiposity and decreases in muscle mass (sarcopenia) have been shown to contribute to disability in late life. Furthermore, there is evidence that obesity-related physiological states, such as insulin resistance and systemic inflammation, may exacerbate physical functioning problems. Both conditions have been shown to prompt hypercatabolism and impair the anabolic effect of muscles, ultimately stimulating protein breakdown and suppressing muscle synthesis. This cross-sectional study investigates whether insulin resistance and inflammation partially account for the associations between decreased physical functioning and sarcopenic obesity. Subjects include 2,287 males and females aged 60 and older without diagnosed diabetes from the National Health and Nutrition Examination Survey (NHANES 1999-2004). Body composition measurements indicating waist circumference and appendicular skeletal muscle mass, measured by dual-energy X-ray absorptiometry (DXA), were used to construct four body composition categories--healthy, sarcopenic nonobese, nonsarcopenic obese, and sarcopenic obese. Physical functioning was measured using self-reports of difficulty performing six activities. The homeostasis model assessment (IR(HOMA)) was used to measure insulin resistance, while inflammatory state was assessed through measurement of serum C-reactive protein (CRP). Modified Poisson regression models were used to examine the association between physical functioning and body composition, and to evaluate whether differences in insulin resistance or inflammation partially explained this relationship. In the analysis, we controlled for possible confounders such as age, education, sex, height, and race/ethnicity. Findings suggest that physical functioning problems are increased in those with sarcopenic obesity, sarcopenic nonobesity and nonsarcopenic obesity. Furthermore, these associations may be influenced by differences in insulin resistance among different body composition phenotypes.