Evidence map›Paper›PMID 37612415›Full record

ArticleDiabetologia2023

Deteriorating beta cell function is the dominant determinant of progression from normal glucose tolerance to prediabetes/diabetes in young women following pregnancy.

Ravi Retnakaran, Chang Ye, Caroline K Kramer, Anthony J Hanley, Philip W Connelly, Mathew Sermer, Bernard Zinman

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Observational
  9. Article
  10. Review
  11. Article
  12. Review
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

7 authors at 2 institutions in 1 country.

Ravi RetnakaranLeadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, ON, Canada. Ravi.Retnakaran@sinaihealth.ca.ORCID 0000-0003-1989-027X
Chang YeLeadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, ON, Canada.
Caroline K KramerLeadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, ON, Canada.
Anthony J HanleyLeadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, ON, Canada.
Philip W ConnellyDivision of Endocrinology, University of Toronto, Toronto, ON, Canada.
Mathew SermerDepartment of Obstetrics and Gynecology, Mount Sinai Hospital, Toronto, ON, Canada.
Bernard ZinmanLeadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, ON, Canada.
Mount Sinai Hospital · CASt. Michael's Hospital · CA

Funding

CIHR MOP-84206CIHR PJT-156286
6 · The paper itself

Abstract

aims/hypothesisExcess adiposity, insulin resistance and beta cell dysfunction each contribute to the development of prediabetes (impaired glucose tolerance and/or impaired fasting glucose)/diabetes but their comparative impact in relation to one another remains uncertain. We thus ranked their contributions to incident dysglycaemia over the first 5 years postpartum in women reflecting the full spectrum of gestational glucose tolerance (spanning normoglycaemia to gestational diabetes) and hence a range of future diabetic risk.

methodsIn this study, 302 women with normal glucose tolerance (NGT) on OGTT at 3 months postpartum underwent repeat OGTT at 1 year, 3 years and 5 years, enabling serial assessment of glucose tolerance, insulin sensitivity/resistance (Matsuda index, HOMA-IR) and beta cell function (insulin secretion-sensitivity index-2 [ISSI-2], insulinogenic index [IGI]/HOMA-IR). Determinants of prediabetes/diabetes were ranked by change in concordance index (CCI) of Cox proportional hazard regression models.

resultsOver 5 years of follow-up, 89 women progressed from NGT to prediabetes/diabetes (progressors). At 3 months postpartum, though all women were normoglycaemic, future progressors had higher fasting glucose (p=0.03) and 2 h glucose (p<0.0001) than non-progressors, coupled with higher BMI (p=0.001), greater insulin resistance (both Matsuda index and HOMA-IR, p≤0.02) and poorer beta cell function (both ISSI-2 and IGI/HOMA-IR, p≤0.006). Unlike their peers, progressors exhibited deteriorating beta cell function from 1 year to 5 years (both p<0.0001). On regression analyses, the dominant determinants of progression to prediabetes/diabetes were time-varying ISSI-2 (change in CCI 25.2%) and IGI/HOMA-IR (13.0%), in contrast to time-varying Matsuda index (2.9%) and HOMA-IR (0.5%). Neither time-varying BMI nor waist were significant predictors after adjustment for beta cell function and insulin sensitivity/resistance. CONCLUSION/

interpretationDeclining beta cell function is the dominant determinant of incident prediabetes/diabetes in young women following pregnancy.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceInsulin-Secreting CellsPrediabetic StateBlood GlucoseFemaleGlucoseGlucose Tolerance TestHumansInsulinPregnancyBlood GlucoseGlucoseInsulinBeta cell dysfunctionInsulin resistanceOverweightPrediabetesWomen’s health

Identifiers

PMID37612415
OpenAlexW4386086781

What Socratic 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 Socratic graph.