Contribution to postprandial hyperglycemia and effect on initial splanchnic glucose clearance of hepatic glucose cycling in glucose-intolerant or NIDDM patients

Peter C. Butler, Robert A. Rizza

Research output: Contribution to journalArticle

115 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)73-81
Number of pages9
JournalDiabetes
Volume40
Issue number1
DOIs
StatePublished - Jan 1991

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Fingerprint Dive into the research topics of 'Contribution to postprandial hyperglycemia and effect on initial splanchnic glucose clearance of hepatic glucose cycling in glucose-intolerant or NIDDM patients'. Together they form a unique fingerprint.

  • Cite this