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Decreased basal, noninsulin-stimulated glucose uptake and metabolism by skeletal soleus muscle isolated from obese-hyperglycemic (ob/ob) mice.
Open accessAbstract
Insulin resistance of diaphragms of ob/ob mice has been repeatedly demonstrated previously both in vitro and in vivo. In the present study, transport and metabolism of glucose with and without insulin stimulation were compared in a skeletal muscle more likely than diaphragm or heart to be representative of the overall striated muscle mass, i.e. isolated soleus muscle. Compared with soleus muscle from lean controls, unstimulated lactate release in the presence of exogenous glucose was depressed from 16.2 to 12.3 nmol/60 min per mg wet wt in soleus from ob/ob mutants; glycolysis was decreased from 6.6 to 3.7 and [14C]glucose oxidation to 14CO2 from 0.90 to 0.33 nmol glucose/60 min per mg wet wt. Uptake of 2-deoxyglucose (2-DOG), both with and without insulin, was very much less for soleus from ob/ob than from lean mice, at 2-DOG concentrations ranging from 0.1 to 10 mM, and in mice of 6-15 wk. When 2-DOG concentration was 1 mM, its basal uptake was 0.53 nmol/30 min per mg wet wt for soleus of ob/ob as against 0.96 for soleus of lean mice. The absolute increment due to 1 mU/ml insulin was 0.49 in muscle of ob/ob as against 1.21 in that of lean mice. When the resistance to insulin action was decreased by pretreatment in vivo by either streptozotocin injection or fasting, the decreased basal 2-DOG uptake of subsequently isolated soleus muscle was not improved. Inhibition of endogenous oxidation of fatty acids by 2-bromostearate, while greatly increasing 14CO2 production from [14C]glucose, did not affect basal [5-3H]glucose metabolism or 2-DOG uptake. It is suggested that transport and/or phosphorylation of glucose under basal, unstimulated conditions are depressed in soleus muscle of ob/ob mice, whether or not resistance to insulin and hyperinsulinemia are also present. Although the origin of the decreased basal glucose uptake remains unknown it might be related to a similar decrease in basal glucose uptake by ventromedial hypothalamic cells, an event presumably resulting in a tendency to hyperphagia. Decreased basal glucose uptake by soleus muscle of ob/ob mice might explain the hyperglycemia, and hence partly the hyperinsulinemia and excessive fat deposition of those animals.
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“In some animal models of obesity such as in obese Zucker rats or ob/ob mice, skeletal muscle shows a metabolic profile characterized by reduced glucose uptake and glucose oxidation, altered partitioning of fatty acids that are incorporated into triglycerides, and reduced oxygen consumption (14 -18).”
From Expression of Mfn2, the Charcot-Marie-Tooth Neuropathy Type 2A Gene, in Human Skeletal Muscle (2005) · cites this paper as [14]
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“In some animal models of obesity such as in obese Zucker rats or ob/ob mice, skeletal muscle shows a metabolic profile characterized by reduced glucose uptake and glucose oxidation, altered partitioning of fatty acids that are incorporated into triglycerides, or oxidized, insulin resistance and reduced oxygen consumption (38-43”
From Mitofusin-2 Determines Mitochondrial Network Architecture and Mitochondrial Metabolism (2003) · cites this paper as [38]
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“The down-regulation of Mfn2 detected in skeletal muscle from obese subjects or obese rats together with the observation that Mfn2 promotes mitochondrial metabolism may explain some of the metabolic alterations observed during obesity and characterized by impaired muscle glucose oxidation and fatty acid oxidation (36-39”
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Metadata
- Authors
- Cuendet, G. S., Loten, E. G., Jeanrenaud, B., & Renold, A. E.
- Affiliations
- University of Geneva (CH)
- Venue
- Journal of Clinical Investigation
- Published
- 1976-11-01
- Volume
- 58
- Issue
- 5
- Pages
- 1078-1088
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC333274
- OpenAlex
- W2055455959
- Cited by
- 162
- References
- 31
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 1 · 2020: 1 · 2018: 2 · 2017: 2 · 2016: 1 · 2013: 2 · 2012: 1
- FWCI
- 4.11
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Funders
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- insulin resistance, ob/ob mice, leptin deficiency, skeletal muscle glucose uptake, soleus muscle, glucose transport, glucose metabolism, glycolysis, glucose oxidation, 2-deoxyglucose uptake, hyperinsulinemia, hyperglycemia, obesity, streptozotocin, fasting, fatty acid oxidation inhibition, ventromedial hypothalamus, glucose phosphorylation, lactate release, glucose transporters, GLUT4, GLUT2, GLUT1
- MeSH terms
- Acetates, Animals, Glucose, Hyperglycemia, Insulin, Insulin Resistance, Lactates, Male, Mice, Inbred C57BL, Muscles, Obesity, Oxidative Phosphorylation, Pyruvates, Mice
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