Cited by 234Metabolism, Diabetes, and CancerAdipokines, Inflammation, and Metabolic DiseasesDiabetes, Cardiovascular Risks, and Lipoproteins

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Decreased kinase activity of insulin receptors from adipocytes of non-insulin-dependent diabetic subjects.

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Freidenberg, G R, Henry, R R, Klein, H H, Reichart, D R, Olefsky, J M·1987·Journal of Clinical Investigation

DOI 10.1172/jci112789PMC PMC424032

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Abstract

The tyrosine kinase activity of the insulin receptor was examined with partially-purified insulin receptors from adipocytes obtained from 13 lean nondiabetics, 14 obese nondiabetics, and 13 obese subjects with non-insulin-dependent diabetes (NIDDM). Incubation of receptors at 4 degrees C with [gamma-32P]ATP and insulin resulted in a maximal 10-12-fold increase in autophosphorylation of the 92-kDa beta-subunit of the receptor with a half maximal effect at 1-3 ng/ml free insulin. Insulin receptor kinase activity in the three experimental groups was measured by means of both autophosphorylation and phosphorylation of the exogenous substrate Glu4:Tyr1. In the absence of insulin, autophosphorylation and Glu4:Tyr1 phosphorylation activities, measured with equal numbers of insulin receptors, were comparable among the three groups. In contrast, insulin-stimulated kinase activity was comparable in the control and obese subjects, but was reduced by approximately 50% in the NIDDM group. These findings indicate that the decrease in kinase activity in NIDDM resulted from a reduction in coupling efficiency between insulin binding and activation of the receptor kinase. The insulin receptor kinase defects observed in NIDDM could be etiologically related to insulin resistance in NIDDM and the pathogenesis of the diabetic state.

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Authors: Freidenberg, G. R., Henry, R. R., Klein, H. H., Reichart, D. R., & Olefsky, J. M.
Affiliations: United States Department of Veterans Affairs (US)
ORCID: Henry, R R
Olefsky, J M
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1987-01-01
Volume: 79
Issue: 1
Pages: 240-250
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci112789
PMC: PMC424032
OpenAlex: W2169226001
Cited by: 234
References: 58
Citations by year: 2026: 1 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 4 · 2017: 2 · 2016: 1 · 2015: 4 · 2014: 4 · 2013: 1 · 2012: 1
FWCI: 11.43
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (AM 33650, 2r01am033651-03, AM-07494)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords: insulin receptor, tyrosine kinase activity, type 2 diabetes, insulin resistance, adipocytes, receptor autophosphorylation, obesity, insulin binding
MeSH terms: Adipose Tissue, Diabetes Mellitus, Type 2, Humans, Insulin, Obesity, Phosphorylation, Protein-Tyrosine Kinases, Receptor, Insulin, Substrate Specificity

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Decreased kinase activity of insulin receptors from adipocytes of non-insulin-dependent diabetic subjects.

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