Evidence map›Paper›PMID 24995977›Full record

ArticleCell2014

Adipsin is an adipokine that improves β cell function in diabetes.

James C Lo, Sanda Ljubicic, Barbara Leibiger, Matthias Kern, Ingo B Leibiger, Tilo Moede, Molly E Kelly, Diti Chatterjee Bhowmick, Incoronata Murano, Paul Cohen and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 225 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
225citing papers in PubMed, 1 pooled it
22.9field-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

225 citing papers in PubMed, 1 synthesis or guideline pooled it, 368 citations in OpenAlex.

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165 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

19 authors at 5 institutions in 4 countries.

James C LoDana-Farber Cancer Institute and the Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
Sanda LjubicicDana-Farber Cancer Institute and the Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Barbara LeibigerThe Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, 17176 Stockholm, Sweden.
Matthias KernDepartment of Medicine, University of Leipzig, Leipzig 04103, Germany.
Ingo B LeibigerThe Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, 17176 Stockholm, Sweden.
Tilo MoedeThe Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, 17176 Stockholm, Sweden.
Molly E KellyDana-Farber Cancer Institute and the Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Diti Chatterjee BhowmickDana-Farber Cancer Institute and the Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Incoronata MuranoDepartment of Experimental and Clinical Medicine, University of Ancona, 60020 Ancona, Italy.
Paul CohenDana-Farber Cancer Institute and the Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
Alexander S BanksDana-Farber Cancer Institute and the Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Melin J KhandekarDana-Farber Cancer Institute and the Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Arne DietrichDepartment of Surgery, University of Leipzig, Leipzig 04103, Germany.
Jeffrey S FlierHarvard Medical School, Boston, MA 02115, USA.
Saverio CintiDepartment of Experimental and Clinical Medicine, University of Ancona, 60020 Ancona, Italy.
Matthias BlüherDepartment of Medicine, University of Leipzig, Leipzig 04103, Germany.
Nika N DanialDana-Farber Cancer Institute and the Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Per-Olof BerggrenThe Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, 17176 Stockholm, Sweden.
Bruce M SpiegelmanDana-Farber Cancer Institute and the Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: bruce_spiegelman@dfci.harvard.edu.
Harvard University · USKarolinska Institutet · SELeipzig University · DEBrigham and Women's Hospital · USOspedali Riuniti di Ancona · IT

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI ANDREW D LUSTER · 1991 to 2026
$35.3M
CONTROL OF ADIPOCYTE GENE EXPRESSION AND PHYSIOLOGYR37DK031405 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI SPIEGELMAN, BRUCE M. · 1996 to 2013
$8.2M
The Dual Role of Pro-apoptotic BAD in Insulin Secretion and Beta Cell SurvivalR01DK078081 · NIDDK · DANA-FARBER CANCER INST · PI Nika N Danial · 2008 to 2026
$5.7M
CONTROL OF LIPOGENIC ENZYME SYNTHESIS IN ADIPOCYTESR01DK031405 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI SPIEGELMAN, BRUCE M. · 1986 to 2018
$2.9M
Regulation of adipose inflammation and metabolic syndrome by adipsin/factor DK08DK097303 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI LO, JAMES C · 2012 to 2016
$784k
NIDDK NIH HHS DK031405NIDDK NIH HHS DK078081NIDDK NIH HHS DK097303NIDDK NIH HHS K08 DK097303NIDDK NIH HHS P30 DK043351NIDDK NIH HHS R01 DK031405NIDDK NIH HHS R01 DK078081NIDDK NIH HHS R37 DK031405
6 · The paper itself

Abstract

A hallmark of type 2 diabetes mellitus (T2DM) is the development of pancreatic β cell failure, which results in insulinopenia and hyperglycemia. We show that the adipokine adipsin has a beneficial role in maintaining β cell function. Animals genetically lacking adipsin have glucose intolerance due to insulinopenia; isolated islets from these mice have reduced glucose-stimulated insulin secretion. Replenishment of adipsin to diabetic mice treated hyperglycemia by boosting insulin secretion. We identify C3a, a peptide generated by adipsin, as a potent insulin secretagogue and show that the C3a receptor is required for these beneficial effects of adipsin. C3a acts on islets by augmenting ATP levels, respiration, and cytosolic free Ca(2+). Finally, we demonstrate that T2DM patients with β cell failure are deficient in adipsin. These findings indicate that the adipsin/C3a pathway connects adipocyte function to β cell physiology, and manipulation of this molecular switch may serve as a therapy in T2DM.

Indexed as

Adipose TissueAnimalsComplement C3aComplement Factor DDiabetes Mellitus, Type 2Diet, High-FatGlucoseHumansInflammationInsulinInsulin-Secreting CellsInsulin SecretionMiceCFD protein, humanComplement C3aComplement Factor Dcomplement factor D, mouseGlucoseInsulin

Identifiers

PMID24995977
PMCPMC4128197
OpenAlexW2013710242

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.