TY - JOUR
T1 - Effect of insulin on oxidation of intracellularly and extracellularly derived glucose in patients with NIDDM
T2 - Evidence for primary defect in glucose transport and/or phosphorylation but not oxidation
AU - Butler, Peter C.
AU - Kryshak, Edward J.
AU - Marsh, Michael
AU - Rizza, Robert A.
PY - 1990/11
Y1 - 1990/11
N2 - Insulin-stimulated glucose oxidation is decreased in patients with non-insulin-dependent diabetes mellitus (NIDDM). It is not known whether this decrease is due to a primary defect in the oxidative pathway or is secondary to impaired glucose transport and/or phosphorylation. To address this issue, glucose oxidation was measured under steady-state conditions at low (∼270 pmol) and high (∼17 μmol) insulin concentrations in seven patients with NIDDM and seven healthy nondiabetic subjects matched for sex, age, and obesity. Glucose oxidation was measured simultaneously by indirect calorimetry and the isotopedilution technique. Although glucose oxidation and nonoxidative storage were lower (P < 0.05) in diabetic than nondiabetic subjects during the low- and high-dose insulin infusions, oxidation of intracellularly derived glucose, estimated by subtracting the rate of oxidation measured isotopically (i.e., glucose oxidation derived from the extracellular space) from that measured by indirect calorimetry (i.e., total glucose oxidation), did not differ in diabetic and nondiabetic subjects during the low-dose insulin infusion (3.3 ± 0.1 vs. 3.0 ± 0.1 μmol·kg-1·min-1). Both techniques provided identical estimates of glucose oxidation during the high-dose insulin infusion. Impaired oxidation of extracellularly but not intracellularly derived glucose strongly suggests that the cause of decreased glucose oxidation in patients with NIDDM is secondary to impaired glucose transport and/or Phosphorylation rather than a primary abnormality in the oxidative pathway.
AB - Insulin-stimulated glucose oxidation is decreased in patients with non-insulin-dependent diabetes mellitus (NIDDM). It is not known whether this decrease is due to a primary defect in the oxidative pathway or is secondary to impaired glucose transport and/or phosphorylation. To address this issue, glucose oxidation was measured under steady-state conditions at low (∼270 pmol) and high (∼17 μmol) insulin concentrations in seven patients with NIDDM and seven healthy nondiabetic subjects matched for sex, age, and obesity. Glucose oxidation was measured simultaneously by indirect calorimetry and the isotopedilution technique. Although glucose oxidation and nonoxidative storage were lower (P < 0.05) in diabetic than nondiabetic subjects during the low- and high-dose insulin infusions, oxidation of intracellularly derived glucose, estimated by subtracting the rate of oxidation measured isotopically (i.e., glucose oxidation derived from the extracellular space) from that measured by indirect calorimetry (i.e., total glucose oxidation), did not differ in diabetic and nondiabetic subjects during the low-dose insulin infusion (3.3 ± 0.1 vs. 3.0 ± 0.1 μmol·kg-1·min-1). Both techniques provided identical estimates of glucose oxidation during the high-dose insulin infusion. Impaired oxidation of extracellularly but not intracellularly derived glucose strongly suggests that the cause of decreased glucose oxidation in patients with NIDDM is secondary to impaired glucose transport and/or Phosphorylation rather than a primary abnormality in the oxidative pathway.
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U2 - 10.2337/diab.39.11.1373
DO - 10.2337/diab.39.11.1373
M3 - Article
C2 - 2121567
AN - SCOPUS:0025175753
SN - 0012-1797
VL - 39
SP - 1373
EP - 1380
JO - Diabetes
JF - Diabetes
IS - 11
ER -