Endocrine Journal
Online ISSN : 1348-4540
Print ISSN : 0918-8959
ISSN-L : 0918-8959
ORIGINALS
Lean mass inversely predicts plasma glucose levels after oral glucose load independent of insulin secretion or insulin sensitivity in glucose intolerance subjects
Jirateep KwankaewSunee SaetungSuwannee ChanprasertyothinRattana LeelawattanaChatchalit Rattarasarn
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2014 Volume 61 Issue 1 Pages 77-83

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Abstract

Muscle mass inversely relates to 2 hours glucose levels after oral glucose load in non-diabetic subjects. A study in glucose intolerance subjects has never been performed. We conducted this study to determine the relationship between muscle mass and glucose level after oral glucose load in glucose intolerance subjects. Sixty Thai subjects, 44 drug-naïve, newly diagnosed type 2 diabetes mellitus and 16 impaired glucose tolerance were studied. The 180 min 75 g oral glucose tolerance test was performed. Total body fat and lean mass were measured by dual-energy x-ray absorptiometry. Insulin sensitivity was determined by insulin sensitivity index using model of Matsuda & DeFronzo. The 1st-phase and total insulin secretion were determined from glucose tolerance data. Pearson correlation and linear regression were used for the analysis. Lean mass was inversely correlated with area-under-curves of glucose 0-180 min (r =-0.320; p=0.013). The relationship was significant after adjustment with age and body-mass-index (r =-0.350; p=0.007). Area-under-curves of glucose 0-180 min was correlated with height (r =-0.282; p=0.029), fasting glucose (r =0.742; p<0.0001), log area-under-curves of insulin 0-180 min (r =-0.258; p=0.047) and log 1st-phase insulin secretion (r =-0.518; p<0.0001). By multivariate analysis, fasting glucose (standardized β=4.54; p<0.001), log 1st-phase insulin secretion (standardized β=-43.09; p=0.005) and lean mass (standardized β=-0.003; p=0.011) were the significant parameters predicting area-under-curves of glucose 0-180 min. In conclusion, lean mass inversely predicted glucose levels after oral glucose load independent of insulin secretion and insulin sensitivity in glucose intolerance subjects.

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© The Japan Endocrine Society
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