Overnight glucose metabolism in obese non‐insulin‐dependent diabetic patients and in healthy lean individuals
- 1 May 1994
- journal article
- Published by Wiley in Clinical Physiology and Functional Imaging
- Vol. 14 (3) , 251-265
- https://doi.org/10.1111/j.1475-097x.1994.tb00383.x
Abstract
Increased fasting hepatic glucose production is present in NIDDM patients, and has been shown to be due to increased gluconeogenesis. In order to determine the contribution of the cycling between glucose and three-carbon compounds (Cori and glucose-alanine cycles) to the increased hepatic glucose production, glucose kinetics measured overnight in seven obese NIDDM patients and six lean healthy subjects with both 6.6 2H glucose and U-13C glucose were determined. At 0500 h obese NIDDM subjects showed a 40% increase in glucose appearance calculated from 6.6 2H glucose, whereas glucose appearance calculated from U-13C glucose was similar compared to lean subjects, indicating increased glucose cycling. Non-oxidative glucose disposal was also increased three-fold in NIDDM patients. Glucose cycling was increased by 111% in NIDDM patients (118 +/- 18 mumole min-1 vs. 56 +/- 11 in controls, P < 0.05) and was positively correlated with plasma glucose concentration (r = 0.831, P < 0.001) and with non-oxidative glucose disposal (r = 0.714, P < 0.01). Four NIDDM patients were studied again after 3 days of insulin therapy. Insulin restored near-normoglycaemia (7.4 +/- 0.8 mmole l-1) and normalized rates of glucose appearance and glucose cycling. It is concluded that increased glucose cycling in obese NIDDM patients accounts for a major part of the increased fasting hepatic glucose production and non-oxidative glucose disposal in obese NIDDM subjects.Keywords
This publication has 30 references indexed in Scilit:
- Lipolysis and gluconeogenesis from glycerol are increased in patients with noninsulin-dependent diabetes mellitusJournal of Clinical Endocrinology & Metabolism, 1992
- Glucose toxicityEndocrine Reviews, 1992
- Intracellular glucose oxidation and glycogen synthase activity are reduced in non-insulin-dependent (type II) diabetes independent of impaired glucose uptake.Journal of Clinical Investigation, 1990
- Sleep-associated fall in glucose disposal and hepatic glucose output in normal humans. Putative signaling mechanism linking peripheral and hepatic eventsDiabetes, 1989
- Effect of hyperinsulinemia on urea pool size and substrate oxidation ratesDiabetes, 1988
- Increased rate of Cori cycle in obese subjects with NIDDM and effect of weight reductionDiabetes, 1988
- Role of lipid oxidation in pathogenesis of insulin resistance of obesity and type II diabetesDiabetes, 1987
- Effect of Severe Burn Injury on Substrate Cycling by Glucose and Fatty AcidsNew England Journal of Medicine, 1987
- The “Dawn Phenomenon” — A Common Occurrence in Both Non-Insulin-Dependent and Insulin-Dependent Diabetes MellitusNew England Journal of Medicine, 1984
- The Dawn Phenomenon, an Early Morning Glucose Rise: Implications for Diabetic Intraday Blood Glucose VariationDiabetes Care, 1981