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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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“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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Items 101–130 of 130
Šedivý, P., Dezortová, M., Drobný, M., Vlasáková, Z., Herynek, V., & Hájek, M. (2018) · Physiological Research · doi:10.33549/physiolres.933745 · Cited by 7
“…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).”
BackgroundToo Much or Too Little? The Double Jeopardy of Subcutaneous Insulin Therapy in Diabetes
Evans, M. L. (2015) · Diabetes · doi:10.2337/dbi15-0003 · Cited by 6
“In diabetes, it is possible that muscle insulin resistance might be more resistant to the effects of peripheral delivery (6).”
BackgroundSchmitz, O., Lund, S. A., Bak, J. F., �rskov, L., Andersen, P. H., M⊘ller, N., Rasmussen, O., Christiansen, J. S., & Pedersen, O. B. (1994) · Acta Diabetologica · doi:10.1007/bf00580757 · Cited by 7
“Previous experiments [ 33-35 ] have suggested abnormalities in the glucose transport system as being an important pathogenetic factor behind the impaired glucose disposal in skeletal muscle of diabetes mellitus.”
MethodAndersen, P. H., Vestergaard, H., Lund, S. A., et al. (1993) · Diabetic Medicine · doi:10.1111/j.1464-5491.1993.tb00151.x · Cited by 6
Pathogenesis of Type 2 Diabetes
Cusi, K. J., & DeFronzo, R. A. (2001) · Comprehensive physiology · doi:10.1002/cphy.cp070237 · Cited by 5
Metabolic Disturbances in Diabetes
Vella, A. V., & Rizza, R. A. (2010) · Wiley eBooks · doi:10.1002/9781444324808.ch13 · Cited by 5
Glucose processing during the intravenous glucose tolerance test
Henriksen, J. E., ALFORD, F. P., Handberg, A., Vaag, A. A., & Beck‐Nielsen, H. (1996) · Metabolism · doi:10.1016/s0026-0495(96)90030-x · Cited by 4
Yki‐Järvinen, H., & McClain, D. A. (2015) · Wiley eBooks · doi:10.1002/9781118387658.ch27 · Cited by 5
Self-citationYki‐Järvinen, H. (2004) · Wiley eBooks · doi:10.1002/0470862092.d0405 · Cited by 4
Self-citationOrigin of the 31P MR signal at 5.3 ppm in patients with critical limb ischemia
Šedivý, P., Dezortová, M., Drobný, M., et al. (2020) · NMR in Biomedicine · doi:10.1002/nbm.4295 · Cited by 3
“However, these Glu-1-P concentrations were obtained from the dry weight of muscle.(31) The cytosolic concentration should be three times lower,(22) and would correspond to approximately 3% to 5% of the Pun signal strength in our subjects.”
BackgroundShort-term effects of growth hormone on myocardial glucose uptake in healthy humans
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“The mechanisms of insulin resistance in skeletal and cardiac muscle are not clear but are thought to involve a defect in membrane transport or the initial intracellular pathways of glycogen formation (1, 7, 39, 51).”
BackgroundHiperandrogenismo en la mujer diabética: rol de la resistencia insulínica y de la hiperinsulinemia
Tejada, G. G.-R. D., & Escobar-Morreale, H. F. (2003) · Endocrinología y Nutrición · doi:10.1016/s1575-0922(03)74555-0 · Cited by 3
Eshiet, E. R. (2010) · ThinkTech (Texas Tech University) · Cited by 3
Metabolic Disturbances in Diabetes
Vella, A. V., & Rizza, R. A. (2016) · Wiley eBooks · doi:10.1002/9781118924853.ch15 · Cited by 3
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“skeletal muscle (SkM)) [3,4] in the development of hyperglycaemia of both type 1 [5,6] and type 2 [7,8] diabetes and animal models of diabetes [4,9–12] are actively debated [13,14].”
BackgroundWohl, P., Krušinová, E., Klementová, M., et al. (2008) · Physiological Research · doi:10.33549/physiolres.931138 · Cited by 2
[Estrogen receptor alpha in obesity and diabetes].
Cahua‐Pablo, J. Á., Flores‐Alfaro, E., & Cruz, M. (2016) · PubMed · Cited by 2
10.1016/b978-1-4160-2911-3.50032-7
(2000) · Time to knit · doi:10.1016/b978-1-4160-2911-3.50032-7 · Cited by 1
Type I Diabetes Mellitus (Insulin‐Dependent Diabetes Mellitus)
Rizza, R. A., Jensen, M. D., & Nair, K. S. (2001) · Comprehensive physiology · doi:10.1002/cphy.cp070236 · Cited by 1
“Glucose oxidation and nonoxidative storage are decreased in proportion to glucose uptake, suggesting that glucose transport and/or phosphorylation are rate limiting (255).”
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Expression of Inflammatory and Insulin Signaling Genes in Acute and Chronic Stress
Witasp, A. (2010) · Figshare
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Kinase cascades in the regulation of glucose homeostasis
Steiler, T. L. (2005) · Figshare
Central Nervous System (CNS) Nutrient Sensing in Diabetes
Chari, M. (2010) · TSpace (University of Toronto)
Running title: Peripheral Insulin Delivery and Hypoglycemia
Gregory, J. M., Kraft, G., Scott, M. F., Neal, D. W., Farmer, B., Hastings, J. R., Allen, E. J., Donahue, E. P., Rivera, N., Winnick, J. J., et al. (2015)
Burant, C. (2000) · Handbook of experimental pharmacology · doi:10.1007/978-3-642-59651-3_15
Pathogenesis of Type 2 Diabetes
Cusi, K. J., & DeFronzo, R. A. (2001) · Comprehensive physiology · doi:10.1002/j.2040-4603.2001.tb01483.x
Influence of Exercise on Protein and Amino Acid Metabolism
Rennie, M. J. (1995) · Comprehensive physiology · doi:10.1002/j.2040-4603.1995.tb01719.x
“…Wolfe and co-workers, using a new technique in exercising man to partition the amount alanine derived from pyruvate synthesis and protein breakdown (292), have shown that exercise does increase net protein breakdown (i.e., promotes negative tissue nitrogen balance), which must eventually cause…”
Glucose Toxicity and Insulin Resistance in NIDDM
Yki‐Järvinen, H. (1997) · Humana Press eBooks · doi:10.1007/978-1-4757-3906-0_11
Self-citation
Metadata
- 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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