The DOI matches its Crossref record; 60 of the 60 references it cites were found in a registry or an index.
Decreased kinase activity of insulin receptors from adipocytes of non-insulin-dependent diabetic subjects.
Open accessAbstract
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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“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 [151]
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1 retracted
Insulin Sensitivity and Insulin Binding to Monocytes in Maturity-Onset Diabetes
Defronzo, R., Deibert, D., Hendler, R., Felig, P., & Soman, V. (1979) · Journal of Clinical Investigation · doi:10.1172/jci109394 · Cited by 188
RetractedBradford, M. M. (1976) · Analytical Biochemistry · doi:10.1016/0003-2697(76)90527-3 · Cited by 255,302
Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance.
National Diabetes Data Group (1979) · Diabetes · doi:10.2337/diab.28.12.1039 · Cited by 4,909
Metabolism of Isolated Fat Cells
Rodbell, M. (1964) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)51687-2 · Cited by 4,647
Human insulin receptor and its relationship to the tyrosine kinase family of oncogenes
Ullrich, A., Bell, J. R., Chen, E. Y., Herrera, R., Petruzzelli, L., Dull, T. J., Gray, A., Coussens, L. M., Liao, Y.-C., Tsubokawa, M., et al. (1985) · Nature · doi:10.1038/313756a0 · Cited by 2,251
METABOLISM OF ISOLATED FAT CELLS. I. EFFECTS OF HORMONES ON GLUCOSE METABOLISM AND LIPOLYSIS.
Rodbell, M. (1964) · PubMed · Cited by 1,387
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Insulin Stimulates the Phosphorylation of the 95,000-Dalton Subunit of Its Own Receptor
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Hotamisligil, G. S., Arner, P., Caro, J. F., Atkinson, R. L., & Spiegelman, B. M. (1995) · Journal of Clinical Investigation · doi:10.1172/jci117936 · Cited by 3,543
Mechanisms of Insulin Action and Insulin Resistance
Petersen, M. C., & Shulman, G. I. (2018) · Physiological Reviews · doi:10.1152/physrev.00063.2017 · Cited by 3,028
Pathogenesis of type 2 diabetes mellitus
DeFronzo, R. A. (2004) · Medical Clinics of North America · doi:10.1016/j.mcna.2004.04.013 · Cited by 1,342
Obesity Is a Fibroblast Growth Factor 21 (FGF21)-Resistant State
Fisher, F. M., Chui, P. C., Antonellis, P. J., Bina, H. A., Kharitonenkov, A., Flier, J. S., & Maratos-Flier, E. (2010) · Diabetes · doi:10.2337/db10-0193 · Cited by 830
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Hotamisligil, G. S. (1999) · Journal of Internal Medicine · doi:10.1046/j.1365-2796.1999.00490.x · Cited by 780
Metadata
- Authors
- Freidenberg, G. R., Henry, R. R., Klein, H. H., Reichart, D. R., & Olefsky, J. M.
- Affiliations
- United States Department of Veterans Affairs (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1987-01-01
- Volume
- 79
- Issue
- 1
- Pages
- 240-250
- ISSN
- 0021-9738 (ISSN-L)
- 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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