Evidence map›Paper›PMID 34986330›Full record

ReviewCell metabolism2022

Why does obesity cause diabetes?

Samuel Klein, Amalia Gastaldelli, Hannele Yki-Järvinen, Philipp E Scherer

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 506 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
506citing papers in PubMed, 6 pooled it
89.5field-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.

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

506 citing papers in PubMed, 6 syntheses or guidelines pooled it, 815 citations in OpenAlex.

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446 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 4 institutions in 3 countries.

Samuel KleinCenter for Human Nutrition, Washington University School of Medicine, St. Louis, MO 63110, USA; Sansum Diabetes Research Institute, Santa Barbara, CA 93105, USA. Electronic address: sklein@wustl.edu.
Amalia GastaldelliInstitute of Clinical Physiology, National Research Council-CNR, Pisa 56100, Italy.
Hannele Yki-JärvinenMinerva Foundation Institute for Medical Research, 00290 Helsinki, Finland; Department of Medicine, University of Helsinki, Helsinki University Hospital, 00290 Helsinki, Finland.
Philipp E SchererTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA; Department of Cell Biology, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.
Istituto di Fisiologia Clinica · ITThe University of Texas Southwestern Medical Center · USUniversity of Helsinki · FIWashington University in St. Louis · US

Funding

WU INSTITUTE OF CLINICAL AND TRANSLATIONAL SCIENCESUL1TR002345 · NCATS · WASHINGTON UNIVERSITY · PI William G. Powderly · 2017 to 2026
$97.8M
Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Brian N Finck · 1999 to 2026
$30.2M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Jennifer Lynn Powers Carson · 2013 to 2026
$27.1M
TRANSGENICS COREP60DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 1986 to 2012
$25.2M
Adiponectin, A Protein Secreted From Adipose TissueR01DK055758 · NIDDK · YESHIVA UNIVERSITY · PI SCHERER, PHILIPP E · 2000 to 2024
$10.9M
Generation of Novel Genetic Tools to Study Cellular Heterogeneity in Adipose TissuesRC2DK118620 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI GUPTA, RANA K, SCHERER, PHILIPP E · 2019 to 2023
$7.0M
White Adipose Tissue Physiology, Mitochondrial Function and AdiponectinR01DK099110 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI PHILIPP E SCHERER · 2013 to 2026
$6.7M
NCATS NIH HHS UL1 TR002345NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P30 DK056341NIDDK NIH HHS P60 DK020579NIDDK NIH HHS R01 DK055758NIDDK NIH HHS R01 DK099110NIDDK NIH HHS RC2 DK118620
6 · The paper itself

Abstract

The accumulation of an excessive amount of body fat can cause type 2 diabetes, and the risk of type 2 diabetes increases linearly with an increase in body mass index. Accordingly, the worldwide increase in the prevalence of obesity has led to a concomitant increase in the prevalence of type 2 diabetes. The cellular and physiological mechanisms responsible for the link between obesity and type 2 diabetes are complex and involve adiposity-induced alterations in β cell function, adipose tissue biology, and multi-organ insulin resistance, which are often ameliorated and can even be normalized with adequate weight loss.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceAdipose TissueAdiposityHumansObesity

Identifiers

PMID34986330
PMCPMC8740746
OpenAlexW4206513048

What OpenQuestion holds

Textmetadata
LicenceTDM
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.