Evidence map›Paper›PMID 32725157›Full record

Observational studyThe Journal of clinical endocrinology and metabolism2020

Pancreatic Steatosis Associates With Impaired Insulin Secretion in Genetically Predisposed Individuals.

Róbert Wagner, Benjamin Assad Jaghutriz, Felicia Gerst, Morgana Barroso Oquendo, Jürgen Machann, Fritz Schick, Markus W Löffler, Silvio Nadalin, Falko Fend, Alfred Königsrainer and 6 more

Open access · hybridAbstract readObservational Study
In one paragraph

Observational study in The Journal of clinical endocrinology and metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
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  10. Mild Mitochondrial Uncoupling for True Ectopic Lipid Disposal.International journal of molecular sciences · 2025
    Review
  11. The Clock is Still Ticking: Tirzepatide and the Myth of Halting the Natural History of Type 2 Diabetes.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025
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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

16 authors at 2 institutions in 1 country.

Róbert WagnerInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Benjamin Assad JaghutrizInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Felicia GerstInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Morgana Barroso OquendoInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Jürgen MachannInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Fritz SchickInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Markus W LöfflerDepartment of General, Visceral and Transplant Surgery, University Hospital Tübingen, Tübingen, Germany.
Silvio NadalinDepartment of General, Visceral and Transplant Surgery, University Hospital Tübingen, Tübingen, Germany.
Falko FendInstitute of Pathology and Neuropathology, University Hospital Tübingen, Tübingen, Germany.
Alfred KönigsrainerDepartment of General, Visceral and Transplant Surgery, University Hospital Tübingen, Tübingen, Germany.
Andreas PeterInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Dorothea Siegel-AxelInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Susanne UllrichInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Hans-Ulrich HäringInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Andreas FritscheInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Martin HeniInstitute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
University Children's Hospital Tübingen · DEGerman Center for Diabetes Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextPancreatic steatosis leading to beta-cell failure might be involved in type 2 diabetes (T2D) pathogenesis.

objectiveWe hypothesized that the genetic background modulates the effect of pancreatic fat on beta-cell function and investigated genotype × pancreatic fat interactions on insulin secretion.

designTwo observational studies.

settingUniversity hospital. PATIENTS OR

participantsA total of 360 nondiabetic individuals with elevated risk for T2D (Tuebingen Family Study [TUEF]), and 64 patients undergoing pancreatectomy (Pancreas Biobank [PB], HbA1c <9%, no insulin therapy).

main outcome measuresInsulin secretion calculated from 5-point oral glucose tolerance test (TUEF) and fasting blood collection before surgery (PB). A genome-wide polygenic score for T2D was computed from 484,788 genotyped variants. The interaction of magnetic resonance imaging-measured and histologically quantified pancreatic fat with the polygenic score was investigated. Partitioned risk scores using genome-wide significant variants were also computed to gain insight into potential mechanisms.

resultsPancreatic steatosis interacted with genome-wide polygenic score on insulin secretion (P = 0.003), which was similar in the replication cohort with histological measurements (P = 0.03). There was a negative association between pancreatic fat and insulin secretion in participants with high genetic risk, whereas individuals with low genetic risk showed a positive correlation between pancreatic fat and insulin secretion. Consistent interactions were found with insulin resistance-specific and a liver/lipid-specific polygenic scores.

conclusionsThe associations suggest that pancreatic steatosis only impairs beta-cell function in subjects at high genetic risk for diabetes. Genetically determined insulin resistance specifically renders pancreatic fat deleterious for insulin secretion.

Indexed as

Adipose TissueAgedBlood GlucoseBody Mass IndexDiabetes Mellitus, Type 2FemaleGenetic Predisposition to DiseaseGlucose Tolerance TestHumansInsulin ResistanceInsulin SecretionMaleMiddle AgedPancreasPancreatic DiseasesBlood Glucosebeta cell functioninsulin secretionnon-alcoholic fatty pancreas diseasepancreatic steatosisprediabetestype 2 diabetes

Identifiers

PMID32725157
PMCPMC7497818
OpenAlexW3045684455

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.