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Cited by 341Metabolism, Diabetes, and CancerDiabetes, Cardiovascular Risks, and LipoproteinsAdipokines, Inflammation, and Metabolic Diseases

Insulin receptor kinase in human skeletal muscle from obese subjects with and without noninsulin dependent diabetes.

Open access
Caro, J F, Sinha, M K, Raju, S M, Ittoop, O, Pories, W J, Flickinger, E G, Meelheim, D, Dohm, G L·1987·Journal of Clinical Investigation
DOI 10.1172/jci112958PMC PMC424378
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Abstract

We have studied the structure and function of the insulin receptors in obese patients with and without noninsulin dependent diabetes mellitus (NIDDM) and in nonobese controls using partially purified receptors from muscle biopsies. Insulin binding was decreased in obesity due to reduced number of binding sites but no differences were observed in insulin binding between obese subjects with or without NIDDM. The structural characteristics of the receptors, as determined by affinity labeling methods and electrophoretic mobility of the beta-subunit, were not altered in obese or NIDDM compared to normal weight subjects. Furthermore, the ability of insulin to stimulate the autophosphorylation of the beta-subunit and the phosphoamino acid composition of the phosphorylated receptor were the same in all groups. However, insulin receptor kinase activity was decreased in obesity using Glu4:Tyr1 as exogenous phosphoacceptor without any appreciable additional defect when obesity was associated with NIDDM. Thus, our data are supportive of the hypothesis that in muscle of obese humans, insulin resistance is partially due to decreased insulin receptors and insulin receptor kinase activity. In NIDDM the defect(s) in muscle is probably distal to the insulin receptor kinase.

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65 of 65 references verified0 citation errors · 0 not checkable

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  • Insulin binding to solubilized receptors from skeletal muscle and liver is normal in obese and lean diabetic individuals.

    “insulin binding to solubilized receptors obtained from skeletal muscle and liver has been shown to be normal in obese and lean diabetic individuals [152, 153, 155].”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [152]

  • Early studies found a modest 20-30% reduction in insulin binding to monocytes and adipocytes from type 2 diabetic patients, but this was not a consistent finding.

    “Early studies have demonstrated a modest 20–30% reduction in insulin binding to monocytes and adipocytes from type 2 diabetic patients, but this has not been a consistent finding [1, 151–154].”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [152]

  • Most but not all investigators found reduced insulin receptor tyrosine kinase activity in skeletal muscle from normal-weight and obese diabetic subjects that cannot be explained by receptor number or binding affinity.

    “Most [1, 7, 152, 153, 156, 161] but not all [155] investigators have found a reduction in tyrosine kinase activity that cannot be explained by alterations in insulin receptor number or insulin receptor binding affinity.”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [152]

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Research works printed but not linked: 3

  1. Sinha, M. K., W. J. Pories, E. G. Flickinger, D. Meelheim, and J. F. Caro. 1987. Insulin receptor kinase activity of adipose tissue from morbidly obese humans with and without noninsulin-dependent diabetes. Diabetes. In press.
  2. Freidenberg, G. R., R. R. Henry, H. H. Klein, D. R. Reichert, and J. M. Olefsky. 1987. Decreased kinase activity of insulin receptors from adipocytes of non-insulin dependent diabetic (NIDDM) subjects. J Clin. Invest. In press.
  3. Avruch, J., R. A. Nemenoff, M. Pierce, Y. C. Kwok, and P. J. Blackshear. 1985. Protein phosphorylation as a mode of insulin action. In Molecular Basis of Insulin Action. M. P. Czech, editor. Plenum Press, New York and London. 263-296.

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Authors
Caro, J. F., Sinha, M. K., Raju, S. M., Ittoop, O., Pories, W. J., Flickinger, E. G., Meelheim, D., & Dohm, G. L.
Affiliations
East Carolina University (US)
ORCID
Pories, W J
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1987-05-01
Volume
79
Issue
5
Pages
1330-1337
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci112958
PMC
PMC424378
OpenAlex
W2104713078
Cited by
341
References
60
Citations by year
2026: 1 · 2024: 6 · 2023: 2 · 2022: 5 · 2021: 6 · 2020: 2 · 2019: 3 · 2018: 3 · 2017: 2 · 2016: 8 · 2015: 5 · 2014: 4 · 2013: 3 · 2012: 6
FWCI
7.58
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institutes of Health (2r01am032585-03)
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 › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
insulin receptor kinase, insulin receptor, skeletal muscle, obesity, type 2 diabetes, insulin resistance, insulin binding, receptor autophosphorylation, receptor beta-subunit, affinity labeling
MeSH terms
Adult, Diabetes Mellitus, Diabetes Mellitus, Type 2, Female, Humans, Insulin, Insulin Resistance, Male, Muscles, Obesity, Phosphorylation, Protein-Tyrosine Kinases, Receptor, Insulin

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