Localization of Rate-Limiting Defect for Glucose Disposal in Skeletal Muscle of Insulin-Resistant Type I Diabetic Patients
Abstract
We searched for metabolic crossover points in muscle glucose metabolite profiles during maintenance of matched glucose fluxes across forearm muscle in insulin-resistant type I (insulin-dependent) diabetic patients and nondiabetic subjects. To classify subjects as insulin sensitive or insulin resistant, whole-body and forearm glucose disposal, oxidative and nonoxidative glucose disposal (indirect calorimetry), and glycogen synthesis (muscle glycogen content in needle biopsies) were measured under euglycemic conditions at two insulin concentrations. Wholebody and forearm muscle glucose disposal were significantly reduced in diabetic patients compared with control subjects. The reduction in total glucose disposal was due to similar relative reductions in oxidative and nonoxidative glucose disposal, pointing toward rate limitation early in glucose metabolism. The defect in nonoxidative glucose disposal was at least partly due to a defect in muscle glycogen synthesis, because muscle glycogen content failed to increase in response to an increase in the plasma insulin concentration in the diabetic patients. The mostinsulin-resistant type 1 diabetic patients were restudied under conditions where, by glucose mass action, whole-body glucose disposal was forced to be similar to that in the control subjects. Matching glucose fluxes in the two groups resulted in similar rates of forearm and whole-body oxidative and nonoxidative glucose disposal and muscle glycogen synthesis, but it did not result in accumulation of free intracellular glucose, glucose-6-phosphate, glucose-1-phosphate, fructose-6-phosphate, or lactate in muscle. These data imply that the rate-limiting defect for glucose disposal in skeletal muscle of type I diabetic patients is at the level of glucose transport.
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Studies in which glucose disposal rates were matched by increasing the glucose or insulin infusion rates provide further support for these findings.
“Further support for these findings comes from studies in which glucose disposal rates were matched by increasing the glucose or insulin infusion rates ([27](#r27), [66](#r66)).”
From Metabolic flexibility and insulin resistance (2008) · cites this paper as [66]
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BackgroundInfluentialRegulation of Muscle Glucose Uptake In Vivo
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“resting, poorly controlled diabetic state involve both compensatory (48, 55) and glucose toxic (38, 39) effects.”
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“[24] H.”
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“…the effect of chronic hyperinsulinemia (Karakelides et al. 2007) or by reduced nutrient delivery due to limited insulin action and glucose transport (Yki-Jarvinen et al. 1990) or as a result of a reduced muscle blood flow and oxygen supply attributable to microangiopathy (Cree-Green et al. 2015).”
Background
- Authors
- Yki-Järvinen, H., Sahlin, K., Ren, J. M., & Koivisto, V. A.
- Affiliations
- Second Department of Medicine, University of Helsinki Finland Department of Clinical Physiology, Huddinge Hospital Stockholm, Sweden
- University of Helsinki (FI)
- ORCID
- Koivisto, Veikko A
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1990-02-01
- Volume
- 39
- Issue
- 2
- Pages
- 157-167
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2075855413
- Cited by
- 131
- References
- 0
- Citations by year
- 2025: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 4 · 2013: 3 · 2012: 1
- FWCI
- 4.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- type 1 diabetes, insulin resistance, glucose transport, nonoxidative glucose disposal, muscle glycogen synthesis, glucose-6-phosphate, glucose-1-phosphate, fructose-6-phosphate, lactate
- MeSH terms
- Adult, Biological Transport, Diabetes Mellitus, Type 1, Glucose, Glycogen, Glycogen Synthase, Humans, Insulin, Insulin Resistance, Metabolic Clearance Rate, Muscles, Oxidation-Reduction
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