CoChat
Sign Up
Cited by 202Adipokines, Inflammation, and Metabolic DiseasesPancreatic function and diabetesDiabetes, Cardiovascular Risks, and Lipoproteins

Insulin Binding in Diabetes: Relationships with Plasma Insulin Levels and Insulin Sensitivity

Olefsky, Jerrold M, Reaven, Gerald M·1977·Diabetes
DOI 10.2337/diab.26.7.680
Open this paper in CoChat — free account

Abstract

Insulin binding to isolated circulating monocytes from normal subjects and adult patients with diabetes was studied. The diabetic subjects were nonketotic, and their degree of glucose intolerance varied from an abnormal oral glucose tolerance test (chemical diabetes) to significant fasting hyperglycemia. The results indicated that patients with chemical diabetes had a 45 per cent decrease in insulin binding to monocytes, and this decrease was secondary to a reduction in the number of receptor sites per cell (normals, 15,000 sites per monocyte versus 8,500 sites per mono-cyte for chemical diabetics). When the individual data from the normal and chemical diabetic subjects were examined, a highly significant inverse correlation was found between the amount of insulin bound and both the fasting plasma insulin level (r = 0.61, P > 0.001) and the incremental insulin area during an oral glucose tolerance test (r = 0.49, P > 0.001). Furthermore, insulin binding was closely and inversely correlated to the degree of insulin resistance (r = 0.65, P > 0.001) among these subjects. Thus, the ability to bind insulin is inversely related to both the plasma insulin level and insulin sensitivity, and chemical diabetics who are insulin-resistant and hyperinsulinemic have a decreased ability to bind insulin. Many patients with fasting hyperglycemia also have decreased insulin binding. However, although as a group these pa tients have fasting hyperinsulinemia, they are hypoinsulinemic in response to a glucose challenge. Thus, inclusion of their data with that of the normal and chemical-diabetic patients enhances the relationship between insulin binding and fasting insulin level (r = 0.68, P > 0.001) but obliterates the relationship between insulin binding and incremental insulin area. Furthermore, in these subjects no significant correlation was found between insulin binding and the degree of insulin resistance (r = 0.19, N.S.), suggesting that all or most of the insulin resistance in these subjects was independent of changes in insulin receptors. In conclusion, (1) if the subjects are taken as a group, in patients with chemical diabetes and in diabetic patients with fasting hyperglycemia, insulin binding to monocytes is decreased; (2) over the entire spectrum of adult, nonketotic diabetes, insulin binding is decreased to monocytes from patients with fasting hyperinsulinemia, while subjects with normal insulin levels have normal insulin binding; (3) the insulin resistance of patients with chemical diabetes may be related to a decrease in insulin receptors, but this does not appear to be the case for patients with fasting hyperglycemia; and (4) plasma insulin levels are inversely related to insulin binding, but it is the basal, not the stimulated levels that are associated with changes in insulin receptors.

Integrity signals

Registry

Crossref · 10.2337/diab.26.7.680

Cites

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • 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 [158]

Cites

Still being checked.

Cited by

Sorted by citations

Related

Authors
Olefsky, J. M., & Reaven, G. M.
Affiliations
Veterans Health Administration (US)
ORCID
Olefsky, Jerrold M
Venue
Diabetes
Publisher
American Diabetes Association
Published
1977-07-01
Volume
26
Issue
7
Pages
680-688
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diab.26.7.680
OpenAlex
W2149124897
Cited by
202
References
0
Citations by year
2026: 1 · 2024: 1 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 4 · 2016: 1 · 2015: 2 · 2013: 1
FWCI
23.37
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • School of Medicine, Stanford University
  • NIH Clinical Center
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
insulin binding, monocytes, insulin receptor, insulin resistance, hyperinsulinemia, fasting hyperglycemia, type 2 diabetes, plasma insulin, oral glucose tolerance test, impaired glucose tolerance, insulin sensitivity, HOMA-IR, insulin resistance index
MeSH terms
Adult, Blood Glucose, Diabetes Mellitus, Female, Glucose Tolerance Test, Humans, Hyperglycemia, Insulin, Insulin Resistance, Male, Middle Aged, Monocytes, Prediabetic State, Protein Binding, Receptor, Insulin

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review