CoChat
Sign Up
Cited by 111Diabetes, Cardiovascular Risks, and LipoproteinsPancreatic function and diabetesMetabolism, Diabetes, and Cancer

Glucose Storage Is a Major Determinant of in Vivo “Insulin Resistance” in Subjects with Normal Glucose Tolerance

LILLIOJA, S., MOTT, D. M., ZAWADZKI, J. K., YOUNG, A. A., ABBOTT, W. G., BOGARDUS, C.·1986·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/jcem-62-5-922
Open this paper in CoChat — free account

Abstract

In vivo "resistance" to the action of insulin on glucose uptake is commonly found in obesity and is characteristic of noninsulin-dependent diabetes mellitus in obese subjects. To investigate the relationship among glucose uptake, glucose oxidation, and nonoxidative glucose disposal (storage) in subjects with normal glucose tolerance, we studied 25 caucasians and 79 southwestern American Indians, including lean and obese subjects in both groups. The euglycemic clamp technique with simultaneous indirect calorimetry was used to determine rates of glucose uptake and glucose oxidation. These studies were performed at two rates of insulin infusion (40 and 400 mU/m2 X min), with resulting mean plasma insulin concentrations of 113 and 1839 microU/ml, respectively. At the lower insulin infusion rate, there was no glucose storage in subjects with a glucose uptake rate of about 2.2 mg/kg fat free mass X min. In contrast, glucose storage accounted for over 45% of the glucose disposal in subjects with glucose uptake rates over 7.0 mg/kg fat free mass X min studied at similar insulin concentrations. At the high insulin infusion rate, over 70% of the difference in glucose uptake between subjects with a low or high capacity for glucose disposal was due to glucose storage. These studies demonstrated that in normal subjects at both physiological and maximally stimulating plasma insulin concentrations, glucose storage is a major factor in distinguishing between those with low or high rates of insulin-mediated glucose disposal. Since glucose storage may be a specifically activated process, we hypothesize that failure to activate glucose storage is a major defect causing in vivo insulin resistance in subjects with normal glucose tolerance.

Integrity signals

Registry

Crossref · 10.1210/jcem-62-5-922

Cites

30 of 30 references verified0 citation errors · 0 not checkable

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?

  • Obese, IGT, and diabetic subjects have severe impairment in insulin-stimulated glycogen synthase that accounts for most of the defect in insulin-mediated whole-body glucose disposal.

    “Obese, IGT, and diabetic subjects have severe impairment in insulin-stimulated glycogen synthase that accounts for the majority of the defect in insulin-mediated whole-body glucose disposal [1, 2, 21, 195, 206–218].”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [208]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
LILLIOJA, S., MOTT, D. M., ZAWADZKI, J. K., YOUNG, A. A., ABBOTT, W. G., & BOGARDUS, C.
Affiliations
National Institutes of Health (US)
ORCID
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
1986-05
Volume
62
Issue
5
Pages
922-927
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
DOI
10.1210/jcem-62-5-922
OpenAlex
W2164895062
Cited by
111
References
30
Citations by year
2024: 2 · 2021: 1 · 2020: 1 · 2018: 2 · 2015: 3 · 2014: 2 · 2013: 1
FWCI
5.16
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • Research Online (University of Wollongong) (submittedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
insulin resistance, glucose storage, glucose uptake, glucose oxidation, glucose disposal, normal glucose tolerance, obesity, type 2 diabetes, insulin infusion, fat-free mass, Native Americans, euglycemic clamp
MeSH terms
Adult, Blood Glucose, Glucose, Glucose Tolerance Test, Humans, Insulin, Insulin Resistance, Male, Obesity, Oxidation-Reduction

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