Oxidative and non-oxidative glucose metabolism in non-obese Type 2 (non-insulin-dependent) diabetic patients
Open accessAbstract
Insulin resistance is a common feature of Type 2 (non-insulin-dependent) diabetes mellitus. This defect in insulin-mediated glucose metabolism could result from a defect in either glucose oxidation or non-oxidative glucose disposal. To examine this question, euglycaemic insulin clamp studies were performed in 16 normal weight Type 2 and 11 age-matched control subjects. In Type 2 diabetic patients the fasting plasma glucose concentration, 8.39 +/- 0.50 mmol/l, was allowed to decline (over 54 +/- 6 min) to 5.33 +/- 0.11 mmol/l before starting the insulin clamp. Total body glucose uptake was significantly decreased in Type 2 diabetic patients vs control subjects (148 +/- 15 vs 264 +/- 25 mg/min.m2, p less than 0.001). Both total glucose oxidation (59 +/- 6 vs 89 +/- 6 mg/min.m2, p less than 0.005) and non-oxidative glucose disposal (89 +/- 15 vs 179 +/- 24 mg/min.m2, p less than 0.005) were significantly reduced in the Type 2 diabetic patients. Basal glucose oxidation was also reduced in the Type 2 diabetic patients (22 +/- 3 vs 38 +/- 5 mg/min.m2, p less than 0.01). In conclusion, during the postabsorptive state and under conditions of euglycaemic hyperinsulinaemia, impairment of glucose oxidation and non-oxidative glucose disposal both contribute to the insulin resistance observed in normal weight Type 2 diabetic patients. Since lipid oxidation was normal in this group of diabetic patients, excessive non-esterified fatty acid oxidation cannot explain the defects in glucose disposal.
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Obese, IGT, and diabetic subjects have severe impairment in insulin-stimulated glycogen synthase that accounts for most of the defect in insulin-mediated whole-body glucose disposal.
“Obese, IGT, and diabetic subjects have severe impairment in insulin-stimulated glycogen synthase that accounts for the majority of the defect in insulin-mediated whole-body glucose disposal [1, 2, 21, 195, 206–218].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [207]
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“Both of these processes are aberrantly affected in type 2 diabetes [5,6].”
BackgroundIndependent effects of obesity and insulin resistance on postprandial thermogenesis in men
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- Authors
- Golay, A., DeFronzo, R. A., Ferrannini, E., Simonson, D. C., Thorin, D., Acheson, K., Thi�baud, D., Curchod, B., J�quier, E., & Felber, J. P.
- Affiliations
- Centre Hospitalier Universitaire Vaudois (CH)
- The University of Texas at San Antonio Health Science Center (US)
- University of Pisa (IT)
- Yale University (US)
- University of Lausanne (CH)
- Clinique de La Source (CH)
- Venue
- Diabetologia
- Published
- 1988-08
- Volume
- 31
- Issue
- 8
- Pages
- 585-591
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2017635412
- Cited by
- 91
- References
- 52
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2022: 2 · 2019: 1 · 2018: 4 · 2015: 3 · 2014: 2 · 2013: 4 · 2012: 2
- FWCI
- 2.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion)
- Funders
- National Science Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- National Institutes of Health (AM 24 092)
- National Institute on Aging (AG00233)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- type 2 diabetes, insulin resistance, glucose oxidation, glucose uptake, lipid oxidation
- MeSH terms
- Blood Glucose, Diabetes Mellitus, Type 2, Fatty Acids, Nonesterified, Female, Glucagon, Glucose, Glycolysis, Humans, Insulin, Insulin Infusion Systems, Male, Middle Aged, Oxygen Consumption, Proteins, Reference Values
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