Glucoregulation and hormonal responses to maximal exercise in non-insulin-dependent diabetes

Kjær, Mette Mandrup; Hollenbeck, C. B.; Frey-Hewitt, B; Galbo, H.; Haskell, W. L.; Reaven, G. M.

doi:10.1152/jappl.1990.68.5.2067

Cited by 145 publications

(140 citation statements)

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“…Studies also show lower VO 2max in type 2 diabetic patients compared with age-matched nondiabetic control subjects (22,60,61). The current study showed that the peak VO 2max in type 2 diabetic subjects with poor glycemic control was lower than weight-matched control subjects, although insulin treatment did not significantly alter this.…”

Section: Discussionsupporting

confidence: 40%

Synthesis Rate of Muscle Proteins, Muscle Functions, and Amino Acid Kinetics in Type 2 Diabetes

et al. 2002

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Improvement of glycemic status by insulin is associated with profound changes in amino acid metabolism in type 1 diabetes. In contrast, a dissociation of insulin effect on glucose and amino acid metabolism has been reported in type 2 diabetes. Type 2 diabetic patients are reported to have reduced muscle oxidative enzymes and VO 2max . We investigated the effect of 11 days of intensive insulin treatment (T 2 D؉) on whole-body amino acid kinetics, muscle protein synthesis rates, and muscle functions in eight type 2 diabetic subjects after withdrawing all treatments for 2 weeks (T 2 D؊) and compared the results with those of weight-matched lean control subjects using stable isotopes of the amino acids. Whole-body leucine, phenylalanine and tyrosine fluxes, leucine oxidation, and plasma amino acid levels were similar in all groups, although plasma glucose levels were significantly higher in T 2 D؊. Insulin treatment reduced leucine nitrogen flux and transamination rates in subjects with type 2 diabetes. Synthesis rates of muscle mitochondrial, sarcoplasmic, and mixed muscle proteins were not affected by glycemic status or insulin treatment in subjects with type 2 diabetes. Muscle strength was also unaffected by diabetes or glycemic status. In contrast, the diabetic patients showed increased tendency for muscle fatigability. Insulin treatment also failed to stimulate muscle cytochrome C oxidase activity in the diabetic patients, although it modestly elevated citrate synthase. In conclusion, improvement of glycemic status by insulin treatment did not alter whole-body amino acid turnover in type 2 diabetic subjects, but leucine nitrogen flux, transamination rates, and plasma ketoisocaproate level were decreased. Insulin treatments in subjects with type 2 diabetes had no effect on muscle mitochondrial protein synthesis and cytochrome C oxidase, a key enzyme for ATP production.

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Section: Discussionsupporting

confidence: 40%

Synthesis Rate of Muscle Proteins, Muscle Functions, and Amino Acid Kinetics in Type 2 Diabetes

et al. 2002

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“…An enhanced post-exercise insulin sensitivity has been demonstrated both for glucose-tolerant individuals and for various insulin-resistant populations, including patients with type 2 diabetes, with the change mainly accounted for by an increase in NOGD [11][12][13]. As glycogen synthesis is the primary pathway of NOGD [1], these changes favour glycogen replenishment after exercise [13,17,[35][36][37].…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of muscle glycogen synthase in recovery from exercise in type 2 diabetes

et al. 2015

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Aims/hypothesis Insulin and exercise stimulate skeletal muscle glycogen synthase (GS) activity by dephosphorylation and changes in kinetic properties. The aim of this study was to investigate the effects of insulin, exercise and post-exercise insulin stimulation on GS phosphorylation, activity and substrate affinity in obesity and type 2 diabetes. Methods Obese men with type 2 diabetes (n=13) and weightmatched controls (n = 14) underwent euglycaemichyperinsulinaemic clamps in the rested state and 3 h after 60 min of cycling (70% maximal pulmonary oxygen uptake [V :O 2max ]) . Biopsies from vastus lateralis muscle were obtained before and after clamps, and before and immediately after exercise. Results Insulin-stimulated glucose uptake was lower in diabetic patients vs obese controls with or without prior exercise. Post exercise, glucose partitioning shifted away from oxidation and towards storage in both groups. Insulin and, more potently, exercise increased GS activity (fractional velocity [FV]) and substrate affinity in both groups. Both stimuli caused dephosphorylation of GS at sites 3a+3b, with exercise additionally decreasing phosphorylation at sites 2+2a. In both groups, changes in GS activity, substrate affinity and dephosphorylation at sites 3a+3b by exercise were sustained 3 h post exercise and further enhanced by insulin. Post exercise, reduced GS activity and substrate affinity as well as increased phosphorylation at sites 2+2a were found in diabetic patients vs obese controls. Conclusions/interpretation Exercise-induced activation of muscle GS in obesity and type 2 diabetes involves dephosphorylation of GS at sites 3a+3b and 2+2a and enhanced substrate affinity, which is likely to facilitate glucose partitioning towards storage. Lower GS activity and increased phosphorylation at sites 2+2a in type 2 diabetes in the recovery period imply an impaired response to exercise.

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“…In the postprandial state, exercise has been demonstrated not to increase HGP in hyperinsulinemic patients with type 2 diabetes (11). In contrast, other studies found similar increases in HGP in patients with type 2 diabetes and in healthy control subjects during moderateintensity exercise (12,13).…”

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confidence: 81%

The Effect of Metformin on Glucose Homeostasis During Moderate Exercise

et al. 2014

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OBJECTIVEWe investigated the role of metformin on glucose kinetics during moderate exercise. RESEARCH DESIGN AND METHODSBefore, during, and after a 45-min bout of exercise at 60% VO 2max , glucose kinetics were determined by isotope tracer technique in patients with type 2 diabetes mellitus with metformin treatment (DM2+Met) or without metformin treatment (DM2) and in healthy control subjects (CON) matched for BMI and age. Glucoregulatory hormones and metabolites were measured throughout the study. RESULTSPlasma glucose concentration was unchanged during exercise in CON but decreased in DM2. No significant change was found in DM2+Met. Hormones and metabolites showed no differences among the groups except for elevated exerciseinduced concentrations of lactate in DM2 (area under the curve [AUC] 31 6 1% vs. CON) and glucagon in DM2 (AUC 5 6 1% vs. DM2+Met). Free fatty acid levels were lower in DM2+Met than in DM2 (AUC 214 6 1%). Absolute values of the baseline glucose rate of appearance (Ra) were elevated in DM2 and DM2+Met, but the increase in glucose Ra relative to baseline was blunted in DM2 (19 6 1%) and DM2+Met (18 6 4%) compared with CON (46 6 4%). Glucose rate of disappearance relative to baseline increased more in CON (31 6 3%) than in DM2 (6 6 1%) and DM2+Met (21 6 2%), showing a small increase caused by metformin. Glucose metabolic clearance rate relative to baseline was similar during exercise in DM2 (33 6 1%) and CON (35 6 3%) but was improved in DM2+Met (37 6 3%) compared with DM2.

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Glucoregulation and hormonal responses to maximal exercise in non-insulin-dependent diabetes

Cited by 145 publications

References 0 publications

Synthesis Rate of Muscle Proteins, Muscle Functions, and Amino Acid Kinetics in Type 2 Diabetes

Synthesis Rate of Muscle Proteins, Muscle Functions, and Amino Acid Kinetics in Type 2 Diabetes

Dysregulation of muscle glycogen synthase in recovery from exercise in type 2 diabetes

The Effect of Metformin on Glucose Homeostasis During Moderate Exercise

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