Evidence map›Paper›PMID 31113756›Full record

ReviewMolecular metabolism2019

What role do fat cells play in pancreatic tissue?

Felicia Gerst, Robert Wagner, Morgana Barroso Oquendo, Dorothea Siegel-Axel, Andreas Fritsche, Martin Heni, Harald Staiger, Hans-Ulrich Häring, Susanne Ullrich

Open access · goldAbstract readReview
In one paragraph

Review in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
8.4field-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

40 citing papers in PubMed, 79 citations in OpenAlex.

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  12. Type 2 diabetes mellitus in adults: pathogenesis, prevention and therapy.Signal transduction and targeted therapy · 2024 · on this map
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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

9 authors at 3 institutions in 1 country.

Felicia GerstGerman Center for Diabetes Research (DZD), Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard Karls University of Tübingen, Tübingen, Germany.
Robert WagnerGerman Center for Diabetes Research (DZD), Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard Karls University of Tübingen, Tübingen, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, and Nephrology, University Hospital Tübingen, Tübingen, Germany.
Morgana Barroso OquendoGerman Center for Diabetes Research (DZD), Tübingen, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, and Nephrology, University Hospital Tübingen, Tübingen, Germany.
Dorothea Siegel-AxelGerman Center for Diabetes Research (DZD), Tübingen, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, and Nephrology, University Hospital Tübingen, Tübingen, Germany.
Andreas FritscheGerman Center for Diabetes Research (DZD), Tübingen, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, and Nephrology, University Hospital Tübingen, Tübingen, Germany.
Martin HeniGerman Center for Diabetes Research (DZD), Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard Karls University of Tübingen, Tübingen, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, and Nephrology, University Hospital Tübingen, Tübingen, Germany.
Harald StaigerGerman Center for Diabetes Research (DZD), Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard Karls University of Tübingen, Tübingen, Germany; Institute of Pharmaceutical Sciences, Department of Pharmacy and Biochemistry, Eberhard Karls University Tübingen, Tübingen, Germany.
Hans-Ulrich HäringGerman Center for Diabetes Research (DZD), Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard Karls University of Tübingen, Tübingen, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, and Nephrology, University Hospital Tübingen, Tübingen, Germany.
Susanne UllrichGerman Center for Diabetes Research (DZD), Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard Karls University of Tübingen, Tübingen, Germany. Electronic address: susanne.ullrich@med.uni-tuebingen.de.
Heinrich Heine University Düsseldorf · DEDeutsches Diabetes-Zentrum e.V. · DEUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt is now generally accepted that obesity is a major risk factor for type 2 diabetes mellitus (T2DM). Hepatic steatosis in particular, as well as visceral and ectopic fat accumulation within tissues, is associated with the development of the disease. We recently presented the first study on isolated human pancreatic adipocytes and their interaction with islets [Gerst, F., Wagner, R., Kaiser, G., Panse, M., Heni, M., Machann, J., et al., 2017. Metabolic crosstalk between fatty pancreas and fatty liver: effects on local inflammation and insulin secretion. Diabetologia 60(11):2240-2251.]. The results indicate that the function of adipocytes depends on the overall metabolic status in humans which, in turn, differentially affects islet hormone release. SCOPE OF REVIEW: This review summarizes former and recent studies on factors derived from adipocytes and their effects on insulin-secreting β-cells, with particular emphasis on the human pancreas. The adipocyte secretome is discussed with a special focus on its influence on insulin secretion, β-cell survival and apoptotic β-cell death. MAJOR

conclusionsHuman pancreatic adipocytes store lipids and release adipokines, metabolites, and pro-inflammatory molecules in response to the overall metabolic, humoral, and neuronal status. The differentially regulated adipocyte secretome impacts on endocrine function, i.e., insulin secretion, β-cell survival and death which interferes with glycemic control. This review attempts to explain why the extent of pancreatic steatosis is associated with reduced insulin secretion in some studies but not in others.

Indexed as

AdipocytesAdipocytes, WhiteAdipokinesAnimalsBlood GlucoseCell DifferentiationCytokinesDiabetes Mellitus, Type 2Fatty LiverHumansInflammationInsulin-Secreting CellsObesityPancreasParacrine CommunicationRisk FactorsAdipokinesBlood GlucoseCytokinesAdipocytesFatty pancreasInsulin secretionParacrine signallingType 2 diabetes mellitus (T2DM)β-cell mass

Identifiers

PMID31113756
PMCPMC6600604
OpenAlexW2944563185

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.