TY - JOUR
T1 - Type I diabetes mellitus does not alter initial splanchnic glucose extraction or hepatic UDP-glucose flux during enteral glucose administration
AU - Vella, A.
AU - Shah, P.
AU - Basu, R.
AU - Basu, A.
AU - Camilleri, M.
AU - Schwenk, W. F.
AU - Rizza, R. A.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2001
Y1 - 2001
N2 - Aims/hypothesis. Our aim was to determine whether an alteration in splanchnic glucose metabolism could contribute to postprandial hyperglycaemia in people with Type I (insulin-dependent) diabetes mellitus. Methods. Splanchnic glucose extraction, hepatic glycogen synthesis and endogenous glucose production were compared in 8 Type I diabetic patients and in 11 control subjects. Endogenous hormone secretion was inhibited with somatostatin while insulin (∼ 550 pmol/1) and glucagon (∼130 ng/1) concentrations were matched with exogenous hormone infusions. Glucose containing [3-3H] glucose was infused into the duodenum at a rate of 20 μmol ·. kg-1 · min-1 Plasma glucose concentrations were maintained at about 8.5 mmol/1 in both groups by means of a separate variable intravenous glucose infusion. Results. Initial splanchnic glucose uptake, calculated by subtracting the systemic rate of appearance of [3-3H] glucose from the rate of infusion of [3-3H] glucose into the duodenum, did not differ in the diabetic and non-diabetic patients (4.1 ± 0.8 vs 3.0 ± 1.0 μmol/kg/min). In addition, hepatic glycogen synthesis, measured using the acetaminophen glucuronide method did not differ (10.7 ± 2.4 vs 10.1 ± 2.7 μmol · kg-1 · min-1). On the other hand, suppression of endogenous glucose production, measured by an intravenous infusion of [6,6-2H2] glucose, was greater (p < 0.05) in the diabetic than in the non-diabetic subjects (1.7 ± 1.6 vs 5.8 ± 1.9 μmol · kg-1 · min-1). Conclusion/interpretation. When glucose, insulin and glucagon concentrations are matched in individuals with relatively good chronic glycaemic control, Type I diabetes does not alter initial splanchnic glucose uptake of enterally delivered glucose or hepatic glycogen synthesis. Alterations in splanchnic glucose metabolism are not likely to contribute to postprandial hyperglycaemia in people with well controlled Type I diabetes.
AB - Aims/hypothesis. Our aim was to determine whether an alteration in splanchnic glucose metabolism could contribute to postprandial hyperglycaemia in people with Type I (insulin-dependent) diabetes mellitus. Methods. Splanchnic glucose extraction, hepatic glycogen synthesis and endogenous glucose production were compared in 8 Type I diabetic patients and in 11 control subjects. Endogenous hormone secretion was inhibited with somatostatin while insulin (∼ 550 pmol/1) and glucagon (∼130 ng/1) concentrations were matched with exogenous hormone infusions. Glucose containing [3-3H] glucose was infused into the duodenum at a rate of 20 μmol ·. kg-1 · min-1 Plasma glucose concentrations were maintained at about 8.5 mmol/1 in both groups by means of a separate variable intravenous glucose infusion. Results. Initial splanchnic glucose uptake, calculated by subtracting the systemic rate of appearance of [3-3H] glucose from the rate of infusion of [3-3H] glucose into the duodenum, did not differ in the diabetic and non-diabetic patients (4.1 ± 0.8 vs 3.0 ± 1.0 μmol/kg/min). In addition, hepatic glycogen synthesis, measured using the acetaminophen glucuronide method did not differ (10.7 ± 2.4 vs 10.1 ± 2.7 μmol · kg-1 · min-1). On the other hand, suppression of endogenous glucose production, measured by an intravenous infusion of [6,6-2H2] glucose, was greater (p < 0.05) in the diabetic than in the non-diabetic subjects (1.7 ± 1.6 vs 5.8 ± 1.9 μmol · kg-1 · min-1). Conclusion/interpretation. When glucose, insulin and glucagon concentrations are matched in individuals with relatively good chronic glycaemic control, Type I diabetes does not alter initial splanchnic glucose uptake of enterally delivered glucose or hepatic glycogen synthesis. Alterations in splanchnic glucose metabolism are not likely to contribute to postprandial hyperglycaemia in people with well controlled Type I diabetes.
KW - Acetaminophen glucuronide
KW - Hepatic glycogen synthesis
KW - Postprandial hyperglycaemia
KW - Splanchnic glucose metabolism
KW - Type I diabetes mellitus
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U2 - 10.1007/s001250051682
DO - 10.1007/s001250051682
M3 - Article
C2 - 11440366
AN - SCOPUS:0034847718
SN - 0012-186X
VL - 44
SP - 729
EP - 737
JO - Diabetologia
JF - Diabetologia
IS - 6
ER -