CoChat
Sign Up
Cited by 85Adipokines, Inflammation, and Metabolic DiseasesDiabetes, Cardiovascular Risks, and LipoproteinsMetabolism, Diabetes, and Cancer

Relationship between in Vivo Insulin Resistance and Decreased Insulin Receptors in Obese Man*

KOLTERMAN, ORVILLE G., REAVEN, GERALD M., OLEFSKY, JERROLD M.·1979·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/jcem-48-3-487
Open this paper in CoChat — free account

Abstract

We have studied the relationship between in vivo insulin sensitivity and in vitro insulin binding to adipocytes in obese and nonobese subjects. Insulin binding studies demonstrated a 40% (P > 0.01) decrease in the number of receptor sites per cell in adipocytes from the obese patients. Insulin sensitivity was assessed by a previously defined technique in which insulin and glucose are constantly administered while endogenous insulin secretion is inhibited by an infusion of epinephrine (6 μg/min) and propranolol (0.08 mg/min). Using this technique, the resulting steady state plasma glucose (SSPG) levels provide a measure of overall in vivo insulin sensitivity. The dose-response relationship between the steady state plasma insulin concentration and glucose disposal was determined by performing three separate infusions on each subject in which the glucose infusion rate was kept constant while the rate of insulin infusion was serially increased in each study. Compared to the normal subjects, the dose-response curves for the obese subjects were markedly shifted to the right. Thus, for any given submaximal plasma insulin level the SSPG level was always greater in the obese patients. However, at the maximal insulin level, the SSPG levels in the obese subjects were reduced to the normal range. Therefore, although the obese patients were insulin resistant at submaximal insulin levels, this insulin resistance could be overcome at higher insulin levels, and this is the predicted functional consequence of a decrease in the number of cellular insulin receptors. In conclusion, 1) obese subjects demonstrate decreased in vivo insulin sensitivity and decreased adipocyte insulin receptors; 2) the in vivo dose-response relationship between plasma insulin and glucose disposal is shifted to the right in obesity; and 3) these data are most consistent with the concept that decreased target tissue insulin receptors are the predominant cause of the overall in vivo insulin resistance in obesity. (J Clin Endocrinol Metab48: 487,1979)

Integrity signals

Registry

Crossref · 10.1210/jcem-48-3-487

Cites

27 of 27 references verified0 citation errors · 0 not checkable

Statistics

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

Claims the paper makes

We couldn’t retrieve this paper’s full text, 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?

Cites

1 retracted

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
KOLTERMAN, O. G., REAVEN, G. M., & OLEFSKY, J. M.
Affiliations
United States Department of Veterans Affairs (US)
ORCID
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
1979-03
Volume
48
Issue
3
Pages
487-494
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
DOI
10.1210/jcem-48-3-487
OpenAlex
W1966090574
Cited by
85
References
27
Citations by year
2024: 1 · 2022: 2 · 2018: 2 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 1 · 2012: 1
FWCI
11.72
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
NIH Clinical Center
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
insulin resistance, obesity, insulin receptor, adipocytes, insulin binding, insulin sensitivity, glucose disposal, dose-response relationship, steady-state plasma glucose
MeSH terms
Adipose Tissue, Blood Glucose, Glucose Tolerance Test, Humans, Insulin, Insulin Resistance, Obesity, 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