TY - JOUR
T1 - Postprandial hyperglycemia in patients with noninsulin-dependent diabetes mellitus. Role of hepatic and extrahepatic tissues
AU - Firth, R. G.
AU - Bell, P. M.
AU - Marsh, H. M.
AU - Hansen, I.
AU - Rizza, R. A.
PY - 1986
Y1 - 1986
N2 - Patients with noninsulin-dependent diabetes mellitus (NIDDM) have both preprandial and postprandial hyperglycemia. To determine the mechanism responsible for the postprandial hyperglycemia, insulin secretion, insulin action, and the pattern of carbohydrate metabolism after glucose ingestion were assessed in patients with NIDDM and in matched nondiabetic subjects using the dual isotope and forearm catheterization techniques. Prior to meal ingestion, hepatic glucose release was increased (P < 0.001) in the diabetic patients measured using [2-3H] or [3-3H]glucose. After meal ingestion, patients with NIDDM had excessive rates of systemic glucose entry (1,316±56 vs. 1,018±65 mg/kg.7 h, P < 0.01), primarily owing to a failure to suppress adequately endogenous glucose release (680±50 vs. 470±32 mg/kg.7 h, P < 0.01) from its high preprandial level. Despite impaired suppression of endogenous glucose production during a hyperinsulinemic glucose clamp (P < 0.001) and decreased postprandial C-peptide response (P < 0.05) in NIDDM, percent suppression of hepatic glucose release after oral glucose was comparable in the diabetic and nondiabetic subjects (45±3 vs. 39±2%). Although new glucose formation from meal-derived three-carbon precursors (53±3 vs. 40±7 mg/kg.7 h, P < 0.05) was greater in the diabetic patients, it accounted for only a minor part of this excessive postprandial hepatic glucose release. Postprandial hyperglycemia was exacerbated by the lack of an appropriate increase in glucose uptake whether measured isotopically or by forearm glucose uptake. Thus as has been proposed for fasting hyperglycemia, excessive hepatic glucose release and impaired glucose uptake are involved in the pathogenesis of postprandial hyperglycemia in patients with NIDDM.
AB - Patients with noninsulin-dependent diabetes mellitus (NIDDM) have both preprandial and postprandial hyperglycemia. To determine the mechanism responsible for the postprandial hyperglycemia, insulin secretion, insulin action, and the pattern of carbohydrate metabolism after glucose ingestion were assessed in patients with NIDDM and in matched nondiabetic subjects using the dual isotope and forearm catheterization techniques. Prior to meal ingestion, hepatic glucose release was increased (P < 0.001) in the diabetic patients measured using [2-3H] or [3-3H]glucose. After meal ingestion, patients with NIDDM had excessive rates of systemic glucose entry (1,316±56 vs. 1,018±65 mg/kg.7 h, P < 0.01), primarily owing to a failure to suppress adequately endogenous glucose release (680±50 vs. 470±32 mg/kg.7 h, P < 0.01) from its high preprandial level. Despite impaired suppression of endogenous glucose production during a hyperinsulinemic glucose clamp (P < 0.001) and decreased postprandial C-peptide response (P < 0.05) in NIDDM, percent suppression of hepatic glucose release after oral glucose was comparable in the diabetic and nondiabetic subjects (45±3 vs. 39±2%). Although new glucose formation from meal-derived three-carbon precursors (53±3 vs. 40±7 mg/kg.7 h, P < 0.05) was greater in the diabetic patients, it accounted for only a minor part of this excessive postprandial hepatic glucose release. Postprandial hyperglycemia was exacerbated by the lack of an appropriate increase in glucose uptake whether measured isotopically or by forearm glucose uptake. Thus as has been proposed for fasting hyperglycemia, excessive hepatic glucose release and impaired glucose uptake are involved in the pathogenesis of postprandial hyperglycemia in patients with NIDDM.
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U2 - 10.1172/JCI112467
DO - 10.1172/JCI112467
M3 - Article
C2 - 3517067
AN - SCOPUS:0022467301
SN - 0021-9738
VL - 77
SP - 1525
EP - 1532
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 5
ER -