TY - JOUR
T1 - Muscle grip strength predicts incident type 2 diabetes
T2 - Population-based cohort study
AU - Li, Joule
AU - Wittert, Gary
AU - Vincent, Andrew
AU - Atlantis, Evan
AU - Shi, Zumin
AU - Appleton, Sarah L.
AU - Hill, Catherine L.
AU - Jenkins, Alicia J.
AU - Januszewski, Andrzej S.
AU - Adams, Robert J.
PY - 2016/6
Y1 - 2016/6
N2 - Objectives To determine the longitudinal relationship of muscle mass and strength with incident type 2 diabetes, and previously unstudied mediating effects of testosterone and inflammation. Methods Community-dwelling male participants (aged ≥ 35 years) of the Men Androgen Inflammation Lifestyle Environment and Stress (MAILES) Study underwent biomedical assessment in 2002-2006 and 2007-2010, including hand grip strength (dynamometer), testosterone and inflammatory markers. Body composition (dual-energy X-ray absorptiometry) was assessed at baseline only. Incident type 2 diabetes was defined as a self-reported doctor diagnosis, diabetes medication use, fasting plasma glucose ≥ 7.0 mmol/L, or glycated haemoglobin ≥ 6.5% (48 mmol/mol) at follow-up, that was not present at baseline. Results Of n = 1632 men, incident type 2 diabetes occurred in 146 (8.9%). Muscle mass was not associated with incident type 2 diabetes. Grip strength was inversely associated with incident type 2 diabetes [unadjusted odds ratio (OR) per 5 kg: 0.87, 95% confidence interval (CI): 0.80-0.95; adjusted OR, 95% CI: 0.87, 0.78-0.97]. Arm muscle quality (grip strength divided by arm lean mass) was similarly associated with incident type 2 diabetes. Testosterone, IL-6 and TNF-α did not significantly mediate the associations. The population attributable fraction of type 2 diabetes from low grip strength was 27% (13-40%), assuming intervention could increase strength by 25%. Conclusions Reduced muscle strength, but not reduced muscle mass, is a risk factor for incident type 2 diabetes in men. This is not mediated by testosterone or inflammation. Intervention could prevent a substantial proportion of disease.
AB - Objectives To determine the longitudinal relationship of muscle mass and strength with incident type 2 diabetes, and previously unstudied mediating effects of testosterone and inflammation. Methods Community-dwelling male participants (aged ≥ 35 years) of the Men Androgen Inflammation Lifestyle Environment and Stress (MAILES) Study underwent biomedical assessment in 2002-2006 and 2007-2010, including hand grip strength (dynamometer), testosterone and inflammatory markers. Body composition (dual-energy X-ray absorptiometry) was assessed at baseline only. Incident type 2 diabetes was defined as a self-reported doctor diagnosis, diabetes medication use, fasting plasma glucose ≥ 7.0 mmol/L, or glycated haemoglobin ≥ 6.5% (48 mmol/mol) at follow-up, that was not present at baseline. Results Of n = 1632 men, incident type 2 diabetes occurred in 146 (8.9%). Muscle mass was not associated with incident type 2 diabetes. Grip strength was inversely associated with incident type 2 diabetes [unadjusted odds ratio (OR) per 5 kg: 0.87, 95% confidence interval (CI): 0.80-0.95; adjusted OR, 95% CI: 0.87, 0.78-0.97]. Arm muscle quality (grip strength divided by arm lean mass) was similarly associated with incident type 2 diabetes. Testosterone, IL-6 and TNF-α did not significantly mediate the associations. The population attributable fraction of type 2 diabetes from low grip strength was 27% (13-40%), assuming intervention could increase strength by 25%. Conclusions Reduced muscle strength, but not reduced muscle mass, is a risk factor for incident type 2 diabetes in men. This is not mediated by testosterone or inflammation. Intervention could prevent a substantial proportion of disease.
KW - skeletal muscle
KW - lean mass
KW - dual energy x-ray absorptiometry
KW - muscle strength
KW - grip strength
KW - Dual energy X-ray absorptiometry
KW - Lean mass
KW - Muscle strength
KW - Grip strength
KW - Skeletal muscle
UR - http://purl.org/au-research/grants/NHMRC/627227
UR - http://www.scopus.com/inward/record.url?scp=84962815286&partnerID=8YFLogxK
U2 - 10.1016/j.metabol.2016.03.011
DO - 10.1016/j.metabol.2016.03.011
M3 - Article
SN - 0026-0495
VL - 65
SP - 883
EP - 892
JO - Metabolism-Clinical and Experimental
JF - Metabolism-Clinical and Experimental
IS - 6
ER -