Evidence mapPaperPMID 39499792Full record

ArticleDiabetes care2025

Effects of Obesity and Hyperglycemia on Postprandial Insulin-Mediated and Non-Insulin-Mediated Glucose Disposal.

Bettina Mittendorfer, Bruce W Patterson, Gordon I Smith, Mihoko Yoshino, Samuel Klein

Abstract read
In one paragraph

Article in Diabetes care, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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

3 citing papers in PubMed.

  1. Trial
  2. Article
  3. 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

5 authors.

Bettina MittendorferCenter for Human Nutrition, Washington University School of Medicine, St. Louis, MO.ORCID 0000-0003-0049-2677
Bruce W PattersonCenter for Human Nutrition, Washington University School of Medicine, St. Louis, MO.
Gordon I SmithCenter for Human Nutrition, Washington University School of Medicine, St. Louis, MO.
Mihoko YoshinoCenter for Human Nutrition, Washington University School of Medicine, St. Louis, MO.
Samuel KleinCenter for Human Nutrition, Washington University School of Medicine, St. Louis, MO.

Funding

Washington University Institute of Clinical and Translational SciencesUL1TR002345 · WASHINGTON UNIVERSITY · 2025 to 2025
$9.3M
Washington University Nutrition Obesity Research CenterP30DK056341 · WASHINGTON UNIVERSITY · 1999 to 2025
$5.7M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · 2022 to 2025
$5.6M
The Washington University Center for Diabetes Translation ResearchP30DK092950 · WASHINGTON UNIVERSITY · 2025 to 2025
$850k
Barnes-Jewish HospitalLonger Life FoundationNCATS NIH HHS UL1 TR000448NCATS NIH HHS UL1 TR002345NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P30 DK056341NIDDK NIH HHS P30 DK092950NIH HHS P30 DK020579
6 · The paper itself

Abstract

objectiveTo evaluate total, insulin-mediated, and non-insulin-mediated glucose disposal (TGD, IMGD, and NIMGD) after ingesting glucose in people with obesity and different glycemic status. RESEARCH DESIGN AND

methodsWe developed and validated a new glucose tracer model in conjunction with an oral glucose tolerance test to determine IMGD, NIMGD, and TGD (sum of IMGD and NIMGD) after glucose ingestion in four groups of people: 1) lean with normal glucose tolerance (NGT), 2) obese with insulin resistance and NGT due to hyperinsulinemia (Ob-NGT group), 3) obese with insulin resistance and impaired glucose tolerance (IGT) due to inadequate hyperinsulinemia (Ob-IGT group), and 4) obese with insulin resistance and type 2 diabetes due to marked insulin insufficiency (Ob-T2D group). In addition, we evaluated the effect of intensive lifestyle therapy (ILT) that caused ∼15% weight loss on IMGD and NIMGD in people with obesity and type 2 diabetes (T2D).

resultsIMGD progressively decreased and NIMGD progressively increased from lean to Ob-NGT to Ob-IGT to Ob-T2D. IMGD accounted for about 70%, 65%, 50%, and 20% of TGD, and NIMGD accounted for ∼40%, 35%, 50%, and 80% of TGD in lean, Ob-NGT, Ob-IGT and Ob-T2D, respectively. Although NIMGD was approximately twofold and approximately threefold higher in Ob-IGT and Ob-T2D compared with Ob-NGT, NIMGD only partially compensated for markedly impaired IMGD in the Ob-IGT and Ob-T2D. ILT in people with obesity and T2D increased IMGD and decreased NIMGD.

conclusionsNIMGD is a major mechanism of postprandial TGD in people with insulin resistance and inadequate insulin secretion.

Indexed as

HyperglycemiaInsulinObesityAdultBlood GlucoseDiabetes Mellitus, Type 2FemaleGlucoseGlucose IntoleranceGlucose Tolerance TestHumansInsulin ResistanceMaleMiddle AgedPostprandial PeriodBlood GlucoseGlucoseInsulin

Identifiers

PMID39499792
PMCPMC11664199

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.