Evidence map›Paper›PMID 24956127›Full record

ArticleEndocrinology2014

Disruption of protein-tyrosine phosphatase 1B expression in the pancreas affects β-cell function.

Siming Liu, Yannan Xi, Ahmed Bettaieb, Kosuke Matsuo, Izumi Matsuo, Rohit N Kulkarni, Fawaz G Haj

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Protein tyrosine phosphatase 1B is a regulator of alpha-actinin4 in the glomerular podocyte.Biochimica et biophysica acta. Molecular cell research · 2024
    Article
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  12. Protein-tyrosine phosphatase 1B substrates and metabolic regulation.Seminars in cell & developmental biology · 2015
    Review
  13. 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

7 authors at 2 institutions in 1 country.

Siming LiuNutrition Department (S.L., Y.X., A.B., K.M., I.M., F.G.H.), University of California Davis, Davis, California 95616; Joslin Diabetes Center (R.N.K.), Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215; and Division of Endocrinology, Diabetes and Metabolism (F.G.H.), Department of Internal Medicine, and Comprehensive Cancer Center, University of California Davis, Sacramento, California 95817.
Yannan Xi
Ahmed Bettaieb
Kosuke Matsuo
Izumi Matsuo
Rohit N Kulkarni
Fawaz G Haj
University of California, Davis · USJoslin Diabetes Center · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
Role of IGF-1 and Insulin Receptors Beta-Cell SurvivalR01DK067536 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 2004 to 2026
$8.0M
Mouse Metabolic Phenotyping Center (MMPC) at UC DavisU24DK092993 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LLOYD, KC KENT · 2011 to 2015
$4.1M
Role of adipose protein-tyrosine phosphatase 1B in glucose homeostasis and body mR01DK090492 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HAJ, FAWAZ GEORGE · 2011 to 2015
$1.7M
Role of T cell protein-tyrosine phosphatase in pancreatic islet functionR01DK095359 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HAJ, FAWAZ GEORGE · 2014 to 2017
$1.4M
Role of Protein-Tyrosine Phosphatase 1B in Pancreatic Islet FunctionR56DK084317 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HAJ, FAWAZ GEORGE · 2010 to 2010
$230k
NIDDK NIH HHS R01 DK067536NIDDK NIH HHS R01 DK090492NIDDK NIH HHS R01DK090492NIDDK NIH HHS R01 DK095359NIDDK NIH HHS R56 DK084317NIDDK NIH HHS R56DK084317NIDDK NIH HHS U24 DK092993PHS HHS DKR0167536
6 · The paper itself

Abstract

Protein-tyrosine phosphatase 1B (PTP1B) is a physiological regulator of glucose homeostasis and energy balance. However, the role of PTP1B in pancreatic endocrine function remains largely unknown. To investigate the metabolic role of pancreatic PTP1B, we generated mice with pancreas PTP1B deletion (panc-PTP1B KO). Mice were fed regular chow or a high-fat diet, and metabolic parameters, insulin secretion and glucose tolerance were determined. On regular chow, panc-PTP1B KO and control mice exhibited comparable glucose tolerance whereas aged panc-PTP1B KO exhibited mild glucose intolerance. Furthermore, high-fat feeding promoted earlier impairment of glucose tolerance and attenuated glucose-stimulated insulin secretion in panc-PTP1B KO mice. The secretory defect in glucose-stimulated insulin secretion was recapitulated in primary islets ex vivo, suggesting that the effects were likely cell-autonomous. At the molecular level, PTP1B deficiency in vivo enhanced basal and glucose-stimulated tyrosyl phosphorylation of EphA5 in islets. Consistently, PTP1B overexpression in the glucose-responsive MIN6 β-cell line attenuated EphA5 tyrosyl phosphorylation, and substrate trapping identified EphA5 as a PTP1B substrate. In summary, these studies identify a novel role for PTP1B in pancreatic endocrine function.

Indexed as

AnimalsFemaleGene Knockout TechniquesGlucoseGlucose IntoleranceInsulinInsulin-Secreting CellsMaleMiceMice, Inbred C57BLMice, KnockoutPancrelipaseProtein Tyrosine Phosphatase, Non-Receptor Type 1GlucoseInsulinPancrelipaseProtein Tyrosine Phosphatase, Non-Receptor Type 1

Identifiers

PMID24956127
PMCPMC4138572
OpenAlexW2157266872

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.