University of Illinois at Chicago
jc%2E2013-2232.pdf (1.01 MB)

Pancreatic beta-cell Function Is a Stronger Predictor of Changes in Glycemic Control After an Aerobic Exercise Intervention Than Insulin Sensitivity

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journal contribution
posted on 2016-04-12, 00:00 authored by Thomas P. J. Solomon, Steven K. Malin, Kristian Karstoft, Sangeeta R. Kashyap, Jacob M. Haus, John P. Kirwan
Context: Understanding intersubject variability in glycemic control following exercise training will help individualize treatment. Objective: Our aim was to determine whether this variability is related to training-induced changes in insulin sensitivity or pancreatic β-cell function. Design, Setting, and Participants: We conducted an observational clinical study of 105 subjects with impaired glucose tolerance or type 2 diabetes. Interventions and Main Outcome Measures: Individual subject changes in fitness (VO2max), glycemia (glycosylated hemoglobin, fasting glucose, oral glucose tolerance test), insulin sensitivity (hyperinsulinemic-euglycemic clamp), oral glucose-stimulated insulin secretion (GSIS), and disposition index (DI) were measured following 12 to 16 weeks of aerobic exercise training. Regression analyses were used to identify relationships between variables. Results: After training, 86% of subjects increased VO2max and lost weight. Glycosylated hemoglobin, fasting glucose, and 2-hour oral glucose tolerance test were reduced in 69%, 62%, and 68% of subjects, respectively, while insulin sensitivity improved in 90% of the participants. Changes in glycemic control were congruent with changes in GSIS such that 66% of subjects had a reduction in first-phase GSIS, and 46% had reduced second-phase GSIS. Training increased first- and second-phase DI in 83% and 74% of subjects. Training-induced changes in glycemic control were related to changes in GSIS (P < .05), but not insulin sensitivity or DI, and training-induced improvements in glycemic control were largest in subjects with greater pretraining GSIS. Conclusions: Intersubject variability in restoring glycemic control following exercise is explained primarily by changes in insulin secretion. Thus, baseline and training-induced changes in β-cell function may be a key determinant of training-induced improvements in glycemic control.


Centre of Inflammation and Metabolism (T.P.J.S., K.K.), Rigshospitalet, Copenhagen 2100, Denmark; Department of Biomedical Sciences (T.P.J.S.), Faculty of Health Sciences, Panum Institute, University of Copenhagen, Copenhagen 2200, Denmark; Departments of Pathobiology (S.K.M., J.P.K.), Cleveland Clinic, Cleveland, Ohio 44195; Department of Endocrinology (S.R.K.), Diabetes, and Metabolism, Cleveland Clinic, Cleveland, Ohio 44195; Department of Kinesiology and Nutrition (J.M.H.), University of Illinois at Chicago, Chicago, Illinois 60612; and Metabolic Translational Research Center (S.R.K., J.P.K.), Endocrinology and Metabolism Institute, Cleveland Clinic, Cleveland, Ohio 44195



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