CoChat
Sign Up
Cited by 494Diabetes, Cardiovascular Risks, and LipoproteinsPancreatic function and diabetesDiabetes Management and Research

Comparison of impedance to insulin-mediated glucose uptake in normal subjects and in subjects with latent diabetes

Open access
Shen, Shiao-Wei, Reaven, Gerald M., Farquhar, John W.·1970·Journal of Clinical Investigation
DOI 10.1172/jci106433PMC PMC322715
Open this paper in CoChat — free accountOpen PDF

Abstract

A technique was devised for a more accurate measurement than has been heretofore possible of one of the factors responsible for hyperglycemia in the complex syndrome of diabetes. This factor is termed impedance and represents the tissues' insensitivity or resistance to insulin-mediated glucose uptake. It was measured by use of steady-state exogenous insulin and glucose infusions during a period of pharmacological suppression of endogenous insulin secretion. Endogenous new glucose production was also inhibited. Impedance as calculated is a direct function of steady-state glucose concentrations, since exogenous insulin concentrations were similar in all studies. Two groups of normal weight subjects were studied. One had maturity onset latent diabetes, and the other (matched for age, weight, and per cent adiposity) was normal. Impedance was closely reproducible in the same individual and remained relatively constant during prolonged infusions. The diabetics had average infusion glucose concentrations (and thus impedance) 68% higher than the normal group, and it is of note that their previously measured glucose intolerance differed by a similar degree; that is, the diabetic's intolerance (as defined by mean weighted plasma glucose response after oral glucose) was 52% greater than that of the normal individuals.

Integrity signals

Registry

Crossref · 10.1172/jci106433

Cites

3 of 3 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?

  • Several laboratories have approached the problem of measuring insulin sensitivity by breaking the feedback relationship, either by pharmacological suppression of pancreatic insulin secretion or by external feedback control (glucose clamp).

    “During the past decade, several laboratories have approached this problem by breaking the feedback relationship, either by pharmacological suppression of pancreatic insulin secretion (10) or by external feedback control (glucose clamp) to circumvent the effect of plasma insulin to change plasma glucose (11).”

    From Physiologic evaluation of factors controlling glucose tolerance in man: measurement of insulin sensitivity and beta-cell glucose sensitivity from the response to intravenous glucose (1981) · cites this paper as [10]

  • Development of techniques to measure insulin-mediated glucose disposal allowed direct confirmation of insulin resistance in individuals matching a noninsulin-dependent diabetes phenotype.

    “In parallel, development of techniques to measure insulin-mediated glucose disposal allowed for direct confirmation of insulin resistance in individuals matching a noninsulin-dependent diabetes phenotype39–41.”

    From 100 years of insulin: celebrating the past, present and future of diabetes therapy (2021) · cites this paper as [41]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Shen, S.-W., Reaven, G. M., & Farquhar, J. W.
Affiliations
Stanford Medicine (US)
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1970-12-01
Volume
49
Issue
12
Pages
2151-2160
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci106433
PMC
PMC322715
OpenAlex
W1999381960
Cited by
494
References
3
Citations by year
2026: 2 · 2025: 7 · 2024: 13 · 2023: 4 · 2022: 9 · 2021: 8 · 2020: 6 · 2019: 13 · 2018: 10 · 2017: 7 · 2016: 10 · 2015: 11 · 2014: 11 · 2013: 10 · 2012: 8
FWCI
8.32
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • U.S. Public Health Service
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
Keywords
insulin resistance, insulin-stimulated glucose uptake, latent diabetes, maturity-onset diabetes, hyperglycemia, impaired glucose tolerance, insulin infusion, glucose infusion, plasma glucose response
MeSH terms
Adult, Antigens, Blood Glucose, Carbon Isotopes, Diabetes Mellitus, Drug Antagonism, Epinephrine, Female, Glucose, Glucose Tolerance Test, Humans, Hyperglycemia, Injections, Intravenous, Insulin, Liver, Male, Methods, Middle Aged, Propranolol, Time Factors, Diabetes Complications

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