Evidence map›Paper›PMID 24201279›Full record

ReviewNature2013

Cooperation between brain and islet in glucose homeostasis and diabetes.

Michael W Schwartz, Randy J Seeley, Matthias H Tschöp, Stephen C Woods, Gregory J Morton, Martin G Myers, David D'Alessio

Open access · greenAbstract readReview
In one paragraph

Review in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed
34.9field-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

157 citing papers in PubMed, 312 citations in OpenAlex.

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  11. Multi-Omics Analysis of a Spontaneous Type 2 Diabetes Model inInternational journal of molecular sciences · 2026
    Article
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  13. Review
  14. The insulin signalling network.Nature metabolism · 2025
    Review
  15. Article
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  20. Review

97 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

7 authors at 4 institutions in 2 countries.

Michael W SchwartzDiabetes and Obesity Center of Excellence, Department of Medicine, University of Washington, Seattle, Washington 98109, USA.
Randy J Seeley
Matthias H Tschöp
Stephen C Woods
Gregory J Morton
Martin G Myers
David D'Alessio
University of Cincinnati · USHelmholtz Zentrum München · DEUniversity of Michigan–Ann Arbor · USUniversity of Washington · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
PILOT STUDY--CLINICAL NUTRITION RESEARCHP30DK035816 · NIDDK · UNIVERSITY OF WASHINGTON · PI Ellen A Schur · 1986 to 2026
$30.4M
Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Novel Brain Mechanisms Controlling Glucose HomeostasisR01DK083042 · NIDDK · UNIVERSITY OF WASHINGTON · PI SCHWARTZ, MICHAEL W · 2008 to 2025
$7.6M
Neuroendocrine Control of Glucose MetabolismR01DK089056 · NIDDK · UNIVERSITY OF WASHINGTON · PI MORTON, GREGORY J · 2011 to 2024
$5.6M
Hypothalamic Inflammation and Energy HomeostasisR01DK090320 · NIDDK · UNIVERSITY OF WASHINGTON · PI SCHWARTZ, MICHAEL W · 2010 to 2014
$1.8M
Dissecting mechanisms of GLP-1 based therapies for Type II DiabetesR01DK093848 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SEELEY, RANDY J · 2012 to 2015
$1.5M
NIDDK NIH HHS DK083042NIDDK NIH HHS DK089053NIDDK NIH HHS DK093848NIDDK NIH HHS P30 DK017047NIDDK NIH HHS P30 DK020572NIDDK NIH HHS P30 DK035816NIDDK NIH HHS R01 DK083042NIDDK NIH HHS R01 DK089056NIDDK NIH HHS R01 DK090320NIDDK NIH HHS R01 DK093848
6 · The paper itself

Abstract

Although a prominent role for the brain in glucose homeostasis was proposed by scientists in the nineteenth century, research throughout most of the twentieth century focused on evidence that the function of pancreatic islets is both necessary and sufficient to explain glucose homeostasis, and that diabetes results from defects of insulin secretion, action or both. However, insulin-independent mechanisms, referred to as 'glucose effectiveness', account for roughly 50% of overall glucose disposal, and reduced glucose effectiveness also contributes importantly to diabetes pathogenesis. Although mechanisms underlying glucose effectiveness are poorly understood, growing evidence suggests that the brain can dynamically regulate this process in ways that improve or even normalize glycaemia in rodent models of diabetes. Here we present evidence of a brain-centred glucoregulatory system (BCGS) that can lower blood glucose levels via both insulin-dependent and -independent mechanisms, and propose a model in which complex and highly coordinated interactions between the BCGS and pancreatic islets promote normal glucose homeostasis. Because activation of either regulatory system can compensate for failure of the other, defects in both may be required for diabetes to develop. Consequently, therapies that target the BCGS in addition to conventional approaches based on enhancing insulin effects may have the potential to induce diabetes remission, whereas targeting just one typically does not.

Indexed as

HomeostasisAnimalsBlood GlucoseBrainDiabetes MellitusGlucoseHumansInsulinIslets of LangerhansBlood GlucoseGlucoseInsulin

Identifiers

PMID24201279
PMCPMC3983910
OpenAlexW2084610168

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.