Evidence map›Paper›PMID 10491414›Full record

ArticleThe Journal of clinical investigation1999

The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus.

C Weyer, C Bogardus, D M Mott, R E Pratley

Registry-linked trialOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02437084 (Relationship Between Insulin Resistance and Statin Induced Type 2 Diabetes, and Integrative Personal Omics Profiling), which is not on this map. Cited by 598 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
598citing papers in PubMed, 4 pooled it
25.8field-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.

NCT02437084 phase4completedstarted 2015, after this paper: background citation

Relationship Between Insulin Resistance and Statin Induced Type 2 Diabetes, and Integrative Personal Omics Profiling

Ran2015Enrolled115Registered outcomes6Posted comparisons6ConditionsHyperlipidemia, Insulin Resistance, Type 2 DiabetesArmsAtorvastatin
PMID 22883507PMID 23219296PMID 25262344PMID 18551118PMID 25754552PMID 27614854PMID 24326527PMID 25634843PMID 31862745PMID 5480843PMID 7988789PMID 9177392other papers from this trial
Open the trial in the graph
3 · Its place in the literature

Who cites it

598 citing papers in PubMed, 4 syntheses or guidelines pooled it, 1,945 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2022
    Guideline
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Trial
  10. Trial
  11. Trial
  12. Trial
  13. Trial
  14. Trial
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Exploring the Role of Kisspeptin in Polycystic Ovary Syndrome and Its Associated Pregnancy Complications.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review

538 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

C WeyerClinical Diabetes and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, Arizona 85016, USA. cweyer@phx.niddk.nih.gov
C Bogardus
D M Mott
R E Pratley
National Institutes of Health · USNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Risk Factors and Etiology of Obesity and Type 2 DiabetesZIADK069015 · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · 2025 to 2025
$364k
Etiology of obesity--Pathophysiological consequencesZ01DK069015 · DIABETES, DIGESTIVE, KIDNEY DISEASES · 1986 to 2005
–
6 · The paper itself

Abstract

The pathogenesis of type 2 diabetes involves abnormalities in insulin action, insulin secretion, and endogenous glucose output (EGO). However, the sequence with which these abnormalities develop and their relative contributions to the deterioration in glucose tolerance remain unclear in the absence of a detailed longitudinal study. We measured insulin action, insulin secretion, and EGO longitudinally in 17 Pima Indians, in whom glucose tolerance deteriorated from normal (NGT) to impaired (IGT) to diabetic over 5.1 +/- 1.4 years. Transition from NGT to IGT was associated with an increase in body weight, a decline in insulin-stimulated glucose disposal, and a decline in the acute insulin secretory response (AIR) to intravenous glucose, but no change in EGO. Progression from IGT to diabetes was accompanied by a further increase in body weight, further decreases in insulin-stimulated glucose disposal and AIR, and an increase in basal EGO. Thirty-one subjects who retained NGT over a similar period also gained weight, but their AIR increased with decreasing insulin-stimulated glucose disposal. Thus, defects in insulin secretion and insulin action occur early in the pathogenesis of diabetes. Intervention to prevent diabetes should target both abnormalities.

Indexed as

Insulin ResistanceAdultAnthropometryDiabetes Mellitus, Type 2FemaleGlucoseGlucose Tolerance TestHumansInsulinInsulin SecretionMaleObesitySex FactorsGlucoseInsulin

Identifiers

PMID10491414
PMCPMC408438
OpenAlexW2077149049

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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 Socratic graph.