In vitro insulin resistance of human adipocytes isolated from subjects with noninsulin-dependent diabetes mellitus.
Open accessAbstract
To assess possible cellular mechanisms of in vitro resistance in noninsulin-dependent diabetes mellitus (NIDDM), maximum insulin-stimulated glucose transport and utilization and insulin binding were measured in adipocytes isolated from weight-matched normal glycemic subjects and patients with NIDDM. Glucose transport rate was determined by measuring the amount of [U-14C]-D-glucose taken up by incubating adipocytes at trace concentrations of glucose (300 nM), and glucose metabolism by estimating the amount of lactate, CO2, triglyceride, and total glucose carbons retained in the cells following incubating at 5.5 mM glucose. Insulin binding was measured at 50, 100, and 200 pM [mono125I-tyrosinyl A14]insulin. Both maximum insulin-stimulated glucose transport and utilization in adipocytes from diabetic subjects were 40% (P less than 0.01) and 32% (P less than 0.05) lower, respectively, than values obtained for subjects with normal glucose tolerance. In addition, the maximum capacity of glucose transport was correlated with the maximum capacity of glucose utilization (r = 0.81, P less than 0.001). Furthermore, fasting plasma glucose concentrations of diabetic subjects were negatively correlated with both maximum insulin-stimulated glucose transport (r = -0.56, P less than 0.05) and glucose utilization (r = -0.67, P less than 0.05). Since basal glucose transport in adipocytes from diabetic subjects was also 33% lower than in adipocytes from normal subjects, there was no change in the relative ability of insulin to stimulate glucose transport. However, there was a 64% decrease in the sensitivity of the glucose transport system to insulin (P less than 0.05), unrelated to concomitant changes in insulin binding. These results demonstrate that both maximal insulin-stimulated glucose transport and utilization, and the sensitivity of the glucose transport system to insulin, was decreased in adipocytes isolated from subjects with NIDDM. These in vitro defects were associated with impaired glucose metabolism in vivo, consistent with the view that the metabolic alterations observed at the cellular level may contribute to the in vivo insulin resistance of NIDDM.
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The approximately 30% reduction in adipocyte insulin signaling lies within the range of differences in insulin sensitivity between obese and lean participants and between diabetic and nondiabetic participants.
“The approximate 30% reduction in cellular insulin signaling in adipocytes induced by 4 nights of sleep restriction lies within the range of the difference in insulin sensitivity in adipocytes from obese versus lean participants (30) and from diabetic patients versus nondiabetic participants (31).”
From Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study (2012) · cites this paper as [30]
A decrease in insulin receptor number cannot be demonstrated in over half of type 2 diabetic subjects, and reduced insulin binding correlates poorly with severity of insulin resistance.
“a decrease in insulin receptor number cannot be demonstrated in over half of type 2 diabetic subjects, and it has been difficult to demonstrate a correlation between reduced insulin binding and the severity of insulin resistance [156–158].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [156]
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 [156]
In insulin-resistant individuals with T2DM, glucose transport activity is severely impaired.
“In insulin resistant individuals with T2DM, glucose transport activity is severely impaired [156, 181, 182, 187–189].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [156]
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References 36 · Cited by 250
Research works printed but not linked: 2
- Arner, P., J. Bolinder, and J. Ostman. 1982. Insulin re- sistance in normoinsulinemic noninsulin-dependent di- abetes mellitus. Eur. J. Clin. Invest. 12(2):2a. (Abstr.)
- Lohnroth, P., M. DiGirolamo, G. Holm, M. Krotkiewski, and U. Smith. 1982. Impaired glucose metabolism but normal insulin sensitivity in adipocytes from type II diabetics. Eur. J. Clin. Invest. 12(2):24a. (Abstr.)
- Authors
- Kashiwagi, A., Verso, M. A., Andrews, J., Vasquez, B., Reaven, G., & Foley, J. E.
- Affiliations
- National Institutes of Health (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1983-10-01
- Volume
- 72
- Issue
- 4
- Pages
- 1246-1254
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC370408
- OpenAlex
- W2120073172
- Cited by
- 250
- References
- 36
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2022: 1 · 2021: 1 · 2020: 2 · 2019: 5 · 2018: 5 · 2017: 3 · 2016: 1 · 2015: 4 · 2014: 3 · 2013: 4 · 2012: 6
- FWCI
- 15.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- insulin resistance, type 2 diabetes, adipocytes, insulin-stimulated glucose transport, glucose utilization, insulin binding, insulin sensitivity, glucose metabolism, fasting blood glucose
- MeSH terms
- Adipose Tissue, Adult, Biological Transport, Diabetes Mellitus, Diabetes Mellitus, Type 2, Female, Glucose, Glucose Tolerance Test, Humans, Insulin, Insulin Resistance, Male, Obesity, Receptor, Insulin
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