Excessive amounts of glucose enter the systemic circulation when patients with non-insulin-dependent diabetes mellitus (NIDDM) eat a carbohydrate-containing meal. To determine the contribution of hepatic glucose cycling (defined as the net effect of glucose/glucose-6-phosphate cycling and uptake and release of glucose from hepatic glycogen) to postprandial hyperglycemia, diabetic, glucose-intolerant, and nondiabetic subjects were fed mixed meals. The meal contained both [2-3H]glucose (an isotope that is extensively detritiated during hepatic glucose cycling) and [6-3H]glucose (an isotope that is not detritiated during hepatic glucose cycling). Of the 50 g of carbohydrate contained in the meal, ∼4–8 g underwent hepatic glucose cycling. Although total cycling of ingested glucose did not differ between diabetic, glucose-intolerant, and nondiabetic subjects (361 ± 67 vs. 494 ± 106 vs. 322 ± 44 μmol · kg−1 · 5 h−1, respectively), the data suggested that hepatic cycling was increased in the diabetic and glucose-intolerant individuals but not in the nondiabetic subjects during the first 2 h after eating. Hepatic cycling during the first 2 h after eating was correlated with the prevailing glucagon concentration (r = 0.6, P < 0.01) and increased (P < 0.05) as hepatic glucose release increased. Hepatic glucose cycling had a marked effect on the measurement of so-called initial splanchnic glucose uptake. Nevertheless, however measured, initial splanchnic glucose uptake was not decreased and, if anything, was increased in diabetic and glucose-intolerant patients. Integrated postprandial hepatic glucose release increased (r < 0.01) with the severity of fasting hyperglycemia. These results indicate that postprandial hyperglycemia in diabetic and glucose-intolerant patients is not due to enhanced hepatic glucose cycling or a lack of uptake of ingested glucose by the splanchnic bed but rather to excessive release of glucose by the liver coupled with a failure of extrahepatic tissues to appropriately increase glucose disposal.
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January 01 1991
Contribution to Postprandial Hyperglycemia and Effect on Initial Splanchnic Glucose Clearance of Hepatic Glucose Cycling in Glucose-Intolerant or NIDDM Patients
Peter C Butler;
Peter C Butler
Department of Endocrinology and Internal Medicine, Mayo Clinic
Rochester, Minnesota
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Robert A Rizza
Robert A Rizza
Department of Endocrinology and Internal Medicine, Mayo Clinic
Rochester, Minnesota
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Address correspondence and reprint requests to Robert Rizza, MD, Endocrine Research Unit, Room 5-164 West Joseph, Mayo Clinic, Rochester, MN 55905.
Diabetes 1991;40(1):73–81
Article history
Received:
April 11 1990
Revision Received:
August 29 1990
Accepted:
August 29 1990
Citation
Peter C Butler, Robert A Rizza; Contribution to Postprandial Hyperglycemia and Effect on Initial Splanchnic Glucose Clearance of Hepatic Glucose Cycling in Glucose-Intolerant or NIDDM Patients. Diabetes 1 January 1991; 40 (1): 73–81. https://doi.org/10.2337/diab.40.1.73
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