Evidence map›Paper›PMID 7860750›Full record

Trial reportThe Journal of clinical investigation1995

Insulin secretion, insulin action, and hepatic glucose production in identical twins discordant for non-insulin-dependent diabetes mellitus.

A Vaag, J E Henriksen, S Madsbad, N Holm, H Beck-Nielsen

Open access · bronzeAbstract readClinical TrialComparative StudyControlled Clinical Trial
In one paragraph

Trial report in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
22.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 211 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. No Association Between a Genetic Variant ofIndian journal of clinical biochemistry : IJCB · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Twins and endocrinology.Indian journal of endocrinology and metabolism · 2014
    Review
  16. Prkar1a in the regulation of insulin secretion.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2012
    Review
  17. Article
  18. Article
  19. Article
  20. T2DM: Why Epigenetics?Journal of nutrition and metabolism · 2011
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

A VaagOdense University Hospital, Department of Endocrinology and Internal Medicine M, Denmark.
J E Henriksen
S Madsbad
N Holm
H Beck-Nielsen
Odense University Hospital · DKHvidovre Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

12 identical twin pairs discordant for non-insulin-dependent diabetes mellitus (NIDDM) were studied for insulin sensitivity (euglycemic insulin clamp, 40 mU/m2 per min), hepatic glucose production (HGP, [3-3H]glucose infusion), and insulin secretion (oral glucose tolerance test and hyperglycemic [12 mM] clamp, including glucagon administration). Five of the nondiabetic twins had normal and seven had impaired glucose tolerance. 13 matched, healthy subjects without a family history of diabetes were included as control subjects. The NIDDM twins were more obese compared with their non-diabetic co-twins. The nondiabetic twins were insulin resistant and had a delayed insulin and C-peptide response during oral glucose tolerance tests compared with controls. Furthermore, the nondiabetic twins had a decreased first-phase insulin response and a decreased maximal insulin secretion capacity during hyperglycemic clamping and intravenous glucagon administration. Nondiabetic twins and controls had similar rates of HGP. Compared with both nondiabetic twins and controls, the NIDDM twins had an elevated basal rate of HGP, a further decreased insulin sensitivity, and a further impaired insulin secretion pattern as determined by all tests. In conclusion, defects of both in vivo insulin secretion and insulin action are present in non- and possibly prediabetic twins who possess the necessary NIDDM susceptibility genes. However, all defects of both insulin secretion and glucose metabolism are expressed quantitatively more severely in their identical co-twins with overt NIDDM.

Indexed as

GluconeogenesisTwins, MonozygoticAgedAge of OnsetBlood GlucoseCholesterolCholesterol, HDLCholesterol, LDLC-PeptideDiabetes MellitusDiabetes Mellitus, Type 2GlucagonGlucose Clamp TechniqueGlucose Tolerance TestGlycated HemoglobinHumansBlood GlucoseCholesterolCholesterol, HDLCholesterol, LDLC-PeptideGlucagonGlycated HemoglobinInsulinTriglyceridesTritium

Identifiers

PMID7860750
PMCPMC295536
OpenAlexW2155904812

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.