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Cited by 61Adipokines, Inflammation, and Metabolic DiseasesCellular transport and secretionDiabetes, Cardiovascular Risks, and Lipoproteins

Defects in Insulin-Receptor Internalization and Processing in Monocytes of Obese Subjects and Obese NIDDM Patients

Trischitta, Vincenzo, Brunetti, Antonio, Chiavetta, Agata, Benzi, Luca, Papa, Vincenzo, Vigneri, Riccardo·1989·Diabetes
DOI 10.2337/diab.38.12.1579
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Abstract

We investigated intracellular processing of the insulin-receptor complex in monocytes from 12 healthy control subjects, 11 obese nondiabetic subjects, and 13 obese patients with non-insulin-dependent diabetes mellitus (NIDDM) by measuring receptor internalization, recovery of cell-surface insulin binding after receptor internalization, and the release of intracellular intact insulin (insulin retroendocytosis). When monocytes from the three groups of subjects were exposed to 100 nM unlabeled insulin for 30 min at 37°C, the subsequent cell-surface 125I-labeled insulin binding was reduced, but the total number of insulin receptors, measured by radioimmunoassay, was not changed. These findings indicate a redistribution of insulin receptors from the surface to the cell interior. Insulin-receptor internalization was significantly lower in monocytes of obese NIDDM patients (mean ± SE 17.8 ± 4.7%) than in obese subjects and healthy control subjects (33.5 ± 4.5%, P < .05, and 34.4 ± 3.7%, P < .02, respectively). Moreover, in downregulated cells, a complete recovery of the initial insulin binding was observed in control subjects but not in obese NIDDM patients or obese nondiabetic subjects. The release of internalized insulin was also reduced in obese NIDDM patients and obese subjects (f1/2 = 49.0 ± 2.4 min, P < .02; 47.4 ± 5.7 min, P < .05; and 32.9 ± 3.8 in NIDDM patients, obese subjects, and control subjects, respectively). In the radioactivity released from monocytes of obese subjects and obese NIDDM patients, the percentage of intact insulin was higher (P < .05) than in control subjects, suggesting reduced intracellular insulin degradation in obese subjects and obese NIDDM patients. This study indicates that insulin-resistant obese subjects and obese NIDDM patients have multiple postbinding defects of the insulin-receptor intracellular processing. Among these defects, decreased insulin-receptor internalization is specifically associated with diabetic patients.

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  • 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 [154]

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Authors
Trischitta, V., Brunetti, A., Chiavetta, A., Benzi, L., Papa, V., & Vigneri, R.
Affiliations
University of Pisa (IT)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
1989-12-01
Volume
38
Issue
12
Pages
1579-1584
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diab.38.12.1579
OpenAlex
W2146002342
Cited by
61
References
0
Citations by year
2026: 1 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 2 · 2016: 1 · 2015: 2 · 2014: 1 · 2013: 3 · 2012: 1
FWCI
1.48
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
  • IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
insulin receptor internalization, monocytes, obesity, type 2 diabetes, insulin receptor down-regulation, receptor recycling
MeSH terms
Diabetes Mellitus, Diabetes Mellitus, Type 2, Female, Humans, Insulin, Kinetics, Male, Middle Aged, Monocytes, Obesity, Protein Processing, Post-Translational, Receptor, Insulin, Reference Values

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