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1 Department of Medicine, University of Rochester School of Medicine, Rochester, NY, USA
* To whom correspondence should be addressed. E-mail: johngerich{at}compuserve.com.
To assess the mechanisms responsible for postprandial hyperglycemia, we used a triple isotope technique (IV 3-H3 glucose and 14C bicarbonate and oral 6, 6 dideutero-glucose) and indirect calorimetry to compare components of glucose release and pathways for glucose disposal in 26 subjects with type 2 diabetes and 15 age-weight-gender matched volunteers without diabetes for six hours following ingestion of a standard meal. We found 1) that the diabetic subjects had greater overall postprandial glucose release into the systemic circulation (98 ± 3 vs 79 ± 4 gm/6 hr, p<0.001) due to both increased endogenous and meal-glucose release; 2) that their greater endogenous glucose release (37 ± 3 vs 20 ± 2 gm/6 hr, p<0.001) was the result of increases in both gluconeogenesis (27 ± 2 vs 15 ± 1 gm/6 hr, p<0.001) and glycogenolysis (10 ± 1 vs 4 ± 2 gm/6 hr, p=0.007); 3) that most (~90%) of the increased glucose release occurred during the initial 90 minutes and was largely due to glucose from the meal (31 ± 2 vs 19 ± 3 gm in the nondiabetic subjects, p<0.001); 4) that although overall tissue glucose uptake, glycolysis and storage were comparable in both groups (p=0.68, 0.47 and 0.28 respectively), glucose clearance (1.2 ± 0.2 vs 3.0 ± 0.2 ml-1. kg-1.min-1, p<0.001) and oxidation (33 ± 3 vs 46 ± 3 gm/6 hr, p=0.004) were reduced whereas nonoxidative glycolysis was increased (29 ± 2 vs 22 ± 2 gm/6 hrs, p=0.04); and finally 5) that net splanchnic glucose storage was reduced ~45% (6.0 ± 0.8 vs 11.0 ± 1.9 gm/6 hrs, p=0.008) as a result of increased glycogen cycling (63 ± 8 vs 28 ± 3%, p=0.03). We conclude 1) that in type 2 diabetes postprandial hyperglycemia occurs as a result of increased glucose release and impaired glucose clearance, 2) that, although hyperglycemia can overcome the effects of impaired insulin secretion and sensitivity on glucose transport, intracellular defects persist so that glucose fluxes through various pathways are altered and glucose may be shunted away from normal sites of storage (e.g. liver and muscle) into other tissues.
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