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Cited by 72Metabolism, Diabetes, and CancerDiabetes, Cardiovascular Risks, and LipoproteinsAdipose Tissue and Metabolism

Glucose metabolism in perfused skeletal muscle. Demonstration of insulin resistance in the obese Zucker rat

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Kemmer, F W, Berger, M, Herberg, L, Gries, F A, Wirdeier, A, Becker, K·1979·Biochemical Journal
DOI 10.1042/bj1780733PMC PMC1186574
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Abstract

1. The effect of insulin (0.5, 10 and 50 munits/ml of perfusate) on glucose uptake and disposal in skeletal muscle was studied in the isolated perfused hindquarter of obese (fa/fa) and lean (Fa/Fa) Zucker rats and Osborne-Mendel rats. 2. A concentration of 0.5 munit of insulin/ml induced a significant increase in glucose uptake (approx. 2.5 mumol/min per 30 g of muscle) in lean Zucker rats and in Osborne-Mendel rats, and 10 munits of insulin/ml caused a further increase to approx. 6 mumol/min per 30 g of muscle; but 50 munits of insulin/ml had no additional stimulatory effect. In contrast, in obese Zucker rats only 10 and 50 munits of insulin/ml had a stimulatory effect on glucose uptake, the magnitude of which was decreased by 50-70% when compared with either lean control group. Since under no experimental condition tested was an accumulation of free glucose in muscle-cell water observed, the data suggest an impairment of insulin-stimulated glucose transport across the muscle-cell membrane in obese Zucker rats. 3. The intracellular disposal of glucose in skeletal muscle of obese Zucker rats was also insulin-insensitive: even at insulin concentrations that clearly stimulated glucose uptake, no effect of insulin on lactate oxidation (nor an inhibitory effect on alanine release) was observed; [14C]glucose incorporation into skeletal-muscle lipids was stimulated by 50 munits of insulin/ml, but the rate was still only 10% of that observed in lean Zucker rats. 4. The data indicate that the skeletal muscle of obese Zucker rats is insulin-resistant with respect to both glucose-transport mechanisms and intracellular pathways of glucose metabolism, such as lactate oxidation. The excessive degree of insulin-insensitivity in skeletal muscle of obese Zucker rats may represent a causal factor in the development of the glucose intolerance in this species.

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  • In some animal models of obesity, 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.

    “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 <i>Mfn2</i>, the Charcot-Marie-Tooth Neuropathy Type 2A Gene, in Human Skeletal Muscle (2005) · cites this paper as [15]

    The Abstract and Discussion support reduced insulin-stimulated glucose uptake and impaired lactate oxidation in skeletal muscle of obese Zucker rats. But the Perfusion experiments section explicitly says oxygen-consumption rates did not differ between groups, contrary to the claim of reduced oxygen consumption. The paper measures glucose incorporation into total lipids, not the claimed partitioning of fatty acids into triglycerides; page numbers were not provided in our copy. (LLM, conf=0.88)

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  • The down-regulation of Mfn2 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, characterized by impaired muscle glucose oxidation and fatty acid oxidation.

    “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”

    From Mitofusin-2 Determines Mitochondrial Network Architecture and Mitochondrial Metabolism (2003) · cites this paper as [39]

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  • In some animal models of obesity such as 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, insulin resistance and reduced oxygen consumption.

    “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 [39]

    The Abstract and Discussion (page numbers not supplied) report reduced insulin-stimulated glucose uptake and insulin resistance in skeletal muscle of obese Zucker rats, along with impaired lactate oxidation. They do not establish the claimed fatty-acid partitioning or reduced oxygen consumption, and the study does not test ob/ob mice. Impaired lactate oxidation is narrower than a general finding of reduced glucose oxidation. (LLM, conf=0.88)

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Cites

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3 of the 44 references couldn’t be matched to a known paper.

Research works printed but not linked: 6

  1. Bittner, D. L. & Manning, J. (1966) Automation in Analytical Chemistry: Technicon Symposium, New York
  2. Bray, G. A. (1977) Fed. Proc. Fed. Am. Soc. Exp. Biol. 36, 148-153
  3. Goldfine, I. D., Smith, G. J., Wong, K. Y. & Jones, A. L. (1977) Proc. Natl. Acad. Sci. U.S.A. 74, 1368-1372
  4. Gries, F. A. (1970) in Adipose Tissue (Jeanrenaud, B. & Hepp, K. D., eds.), pp. 167-174, Thieme, Stuttgart
  5. Ruderman, N. B. (1971) Ph.D. Thesis, University of Oxford
  6. Zucker, L. M. & Antoniades, H. N. (1972) Endocrinology 90, 1320-1330 Vol. 178

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Authors
Kemmer, F. W., Berger, M., Herberg, L., Gries, F. A., Wirdeier, A., & Becker, K.
Affiliations
University of Toronto (CA)
ORCID
Berger, M
Venue
Biochemical Journal
Publisher
Portland Press Ltd.
Published
1979-03-15
Volume
178
Issue
3
Pages
733-741
ISSN
0264-6021 (ISSN-L)
DOI
10.1042/bj1780733
PMC
PMC1186574
OpenAlex
W1793330704
Cited by
72
References
44
Citations by year
2024: 1 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 1 · 2012: 3
FWCI
1.42
Type
journal article
Language
en
Open access
Locations
  • Biochemical Journal (publishedVersion)
  • PubMed Central (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 › Physiology › Adipose Tissue and Metabolism
Keywords
insulin resistance, skeletal muscle, glucose uptake, glucose transport, glucose metabolism, Zucker fatty rats, Osborne-Mendel rats, insulin-stimulated glucose transport, lactate oxidation, impaired glucose tolerance, insulin dose-response
MeSH terms
Adipose Tissue, Animals, Body Composition, Diabetes Mellitus, Female, Glucose, Glycogen, Insulin, Insulin Resistance, Muscles, Obesity, Perfusion, Rats, In Vitro Techniques

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