Evidence map›Paper›PMID 25126397›Full record

ReviewWorld journal of diabetes2014

SH2B1 regulation of energy balance, body weight, and glucose metabolism.

Liangyou Rui

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 9% 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

58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 90 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Central leptin pathways in metabolic homeostasis.Clinical science (London, England : 1979) · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article
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

1 author at 1 institution in 1 country.

Liangyou RuiLiangyou Rui, Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, United States.
University of Michigan · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID P OLSON · 2013 to 2026
$24.3M
Role of SH2-B in Glucose MetabolismR01DK065122 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUI, LIANGYOU · 2004 to 2012
$2.9M
Transcriptional Regulation of MetabolismR01DK094014 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUI, LIANGYOU · 2012 to 2015
$1.5M
Role of inflammation and cellular stress in the pathogenesis of type 2 diabetesR01DK091591 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUI, LIANGYOU · 2012 to 2015
$1.5M
NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK065122NIDDK NIH HHS R01 DK091591NIDDK NIH HHS R01 DK094014
6 · The paper itself

Abstract

The Src homology 2B (SH2B) family members (SH2B1, SH2B2 and SH2B3) are adaptor signaling proteins containing characteristic SH2 and PH domains. SH2B1 (also called SH2-B and PSM) and SH2B2 (also called APS) are able to form homo- or hetero-dimers via their N-terminal dimerization domains. Their C-terminal SH2 domains bind to tyrosyl phosphorylated proteins, including Janus kinase 2 (JAK2), TrkA, insulin receptors, insulin-like growth factor-1 receptors, insulin receptor substrate-1 (IRS1), and IRS2. SH2B1 enhances leptin signaling by both stimulating JAK2 activity and assembling a JAK2/IRS1/2 signaling complex. SH2B1 promotes insulin signaling by both enhancing insulin receptor catalytic activity and protecting against dephosphorylation of IRS proteins. Accordingly, genetic deletion of SH2B1 results in severe leptin resistance, insulin resistance, hyperphagia, obesity, and type 2 diabetes in mice. Neuron-specific overexpression of SH2B1β transgenes protects against diet-induced obesity and insulin resistance. SH2B1 in pancreatic β cells promotes β cell expansion and insulin secretion to counteract insulin resistance in obesity. Moreover, numerous SH2B1 mutations are genetically linked to leptin resistance, insulin resistance, obesity, and type 2 diabetes in humans. Unlike SH2B1, SH2B2 and SH2B3 are not required for the maintenance of normal energy and glucose homeostasis. The metabolic function of the SH2B family is conserved from insects to humans.

Indexed as

Energy balanceFood intakeGlucose intoleranceHyperphagiaHypothalamusInsulin resistanceLeptin resistanceNonalcoholic fatty liver diseaseObesityType 2 diabetes

Identifiers

PMID25126397
PMCPMC4127586
OpenAlexW2052281855

What Socratic holds

Textmetadata
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 Socratic graph.