CoChat
Sign Up
Cited by 807Pancreatic function and diabetesDiabetes, Cardiovascular Risks, and LipoproteinsDiet, Metabolism, and Disease

Early Metabolic Defects in Persons at Increased Risk for Non-Insulin-Dependent Diabetes Mellitus

Eriksson, Johan, Franssila-Kallunki, Anja, Ekstrand, Agneta, Saloranta, Carola, Widén, Elisabeth, Schalin, Camilla, Groop, Leif·1989·New England Journal of Medicine
DOI 10.1056/nejm198908103210601
Open this paper in CoChat — free account

Abstract

To identify early metabolic abnormalities in non-insulin-dependent diabetes mellitus (NIDDM), we measured sensitivity to insulin and insulin secretion in 26 first-degree relatives of patients with NIDDM and compared these subjects both with 14 healthy control subjects with no family history of NIDDM and with 19 patients with NIDDM. The euglycemic insulin-clamp technique, indirect calorimetry, and infusion of [3-3H]glucose were used to assess insulin sensitivity. Total-body glucose metabolism was impaired in the first-degree relatives as compared with the controls (P less than 0.01). The defect in glucose metabolism was almost completely accounted for by a defect in nonoxidative glucose metabolism (primarily the storage of glucose as glycogen). The relatives with normal rates of metabolism (mean +/- SEM, 1.81 +/- 0.27 mg per kilogram of body weight per minute) and impaired rates (1.40 +/- 0.22 mg per kilogram per minute) in oral glucose-tolerance tests had the same degree of impairment in glucose storage as compared with healthy control subjects (3.76 +/- 0.55 mg per kilogram per minute; P less than 0.01 for both comparisons). During hyperglycemic clamping, first-phase insulin secretion was lacking in patients with NIDDM (P less than 0.01) and severely impaired in their relatives with impaired glucose tolerance (P less than 0.05) as compared with control subjects; insulin secretion was normal in the relatives with normal glucose tolerance. We conclude that impaired glucose metabolism is common in the first-degree relatives of patients with NIDDM, despite their normal results on oral glucose-tolerance tests. Both insulin resistance and impaired insulin secretion are necessary for the development of impaired glucose tolerance in these subjects.

Integrity signals

Registry

Crossref · 10.1056/nejm198908103210601

Cites

47 of 47 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?

  • Re-examination of data from some other studies of high-risk NGT subjects suggests that conclusions disputing the presence of beta-cell dysfunction are erroneous because no difference in insulin responses existed between groups despite insulin resistance, indicating impaired beta-cell adaptation.

    “Thus, re-examination of data from some other studies of high risk subjects with NGT would suggest that the conclusions in those papers disputing the presence of beta-cell dysfunction are erroneous because no difference in the insulin responses existed between groups despite the presence of insulin resistance, indicating impaired beta-cell adaptation [108, 109, 110, 111, 112, 113, 114].”

    From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [112]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Eriksson, J., Franssila-Kallunki, A., Ekstrand, A., Saloranta, C., Widén, E., Schalin, C., & Groop, L.
Affiliations
Helsinki University Hospital (FI)
ORCID
Venue
New England Journal of Medicine
Publisher
Massachusetts Medical Society
Published
1989-08-10
Volume
321
Issue
6
Pages
337-343
ISSN
  • 0028-4793 (ISSN-L)
  • 1533-4406
DOI
10.1056/nejm198908103210601
OpenAlex
W2330505590
Cited by
807
References
47
Citations by year
2026: 1 · 2025: 3 · 2024: 6 · 2023: 5 · 2022: 5 · 2021: 4 · 2020: 8 · 2019: 6 · 2018: 8 · 2017: 17 · 2016: 6 · 2015: 10 · 2014: 11 · 2013: 11 · 2012: 15
FWCI
44.51
Type
journal article
Language
en
Open access
closed
Locations
  • New England Journal of Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Keywords
type 2 diabetes, insulin resistance, impaired insulin secretion, first-degree relatives, familial risk, impaired glucose tolerance, glucose metabolism, glycogen storage, hyperglycemic clamp, hyperinsulinemic-euglycemic clamp, nonoxidative glucose metabolism
MeSH terms
Insulin Secretion, Adult, Blood Glucose, Diabetes Mellitus, Type 2, Female, Gluconeogenesis, Glucose Tolerance Test, Humans, Insulin, Male, Middle Aged, Risk, Glucose Clamp Technique, Lipid Metabolism

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