Literature DB >> 26698153

Obesity is associated with insulin resistance but not skeletal muscle dysfunction or all-cause mortality.

Jeremy P Loenneke1, Paul D Loprinzi2.   

Abstract

Recent work has found that older adults with obesity and systemic inflammation have associated metabolic dysfunction but do not have associated lower lean mass or strength. However, this lean mass estimate may be inflated with obesity, given that 15 % of adipose tissue is composed of fat-free tissue. The primary purpose of this study was to investigate, in a nationally representative sample of adults, whether obese adults with chronic systemic inflammation (unhealthy) have differences in lean mass, muscle strength, and insulin resistance when compared to normal weight individuals without elevated levels of systemic inflammation (healthy). A secondary objective was to determine whether these potential differences were moderated by physical activity and to determine if these groups had a differential risk for all-cause mortality. Our findings suggests that the unhealthy group was associated with higher upper body lean mass (β = 823; 95 % confidence interval (CI) 637-1010; P < 0.001), lower body lean mass (β = 2724; 95 % CI 2291-3158; P < 0.001), and strength (β = 34.6; 95 % CI 13.5-55.7; P = 0.003) compared to the healthy group despite having systemic inflammation and correcting for fat-free adipose tissue. However, the unhealthy group was associated with insulin resistance (odds ratio (OR) = 16.1; 95 % CI 2.7-96.1; P = 0.005) although this finding was attenuated in those physically active (OR = 8.5; 95 % CI 2.43-30.15; P = 0.003). Despite this metabolic dysfunction, there was no difference in all-cause mortality risk between groups (hazard ratio (HR) = 1.16 (95 % CI 0.69-1.96; P = 0.54)) suggesting that higher amounts of lean mass and strength may be protective of premature mortality.

Entities:  

Keywords:  Muscle function; Muscle size; Obesity

Mesh:

Year:  2015        PMID: 26698153      PMCID: PMC5005886          DOI: 10.1007/s11357-015-9865-y

Source DB:  PubMed          Journal:  Age (Dordr)        ISSN: 0161-9152


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