Evidence map›Paper›PMID 17724080›Full record

ArticleMolecular and cellular biology2007

Improved glucose homeostasis in mice with muscle-specific deletion of protein-tyrosine phosphatase 1B.

Mirela Delibegovic, Kendra K Bence, Nimesh Mody, Eun-Gyoung Hong, Hwi Jin Ko, Jason K Kim, Barbara B Kahn, Benjamin G Neel

Registry-linked trialAbstract read
In one paragraph

Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03065140 (Muscle Fat Compartments and Turnover as Determinant of Insulin Sensitivity - the MISTY Study), which is not on this map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
–field-weighted citation impact
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.

NCT03065140 nacompletednot on this mapstarted 2016, after this paper: background citation

Muscle Fat Compartments and Turnover as Determinant of Insulin Sensitivity - the MISTY Study

TypeinterventionalSponsorUniversity of AberdeenRan2016 to 2019Enrolled50ConditionsDiabetesArmsTraining or detraining
3 · Its place in the literature

Who cites it

91 citing papers in PubMed.

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31 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

8 authors.

Mirela DelibegovicCancer Biology Program, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. m.delibegovic@abdn.ac.uk
Kendra K Bence
Nimesh Mody
Eun-Gyoung Hong
Hwi Jin Ko
Jason K Kim
Barbara B Kahn
Benjamin G Neel

Funding

Transgenic CoreP30DK057521 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI FLOREZ, JOSE CARLOS · 2000 to 2019
$31.4M
Transgenic CoreP30DK046200 · NIDDK · TUFTS MEDICAL CENTER · PI GREENBERG, ANDREW S, PERISSI, VALENTINA · 1992 to 2021
$25.0M
Role of PTP1B in Body Mass RegulationR01DK060838 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 2002 to 2011
$3.8M
Protein Tyrosine Phosphatase 1B and Insulin ActionR01DK060839 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B · 2002 to 2005
$1.7M
Interleukin-10 and Regulation of Skeletal Muscle Insulin ActionR01DK080756 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KIM, JASON K · 2008 to 2012
$1.6M
NIDDK NIH HHS 5-P30-DK046200NIDDK NIH HHS DK 60838NIDDK NIH HHS DK 60839NIDDK NIH HHS P30 DK046200NIDDK NIH HHS P30 DK057521NIDDK NIH HHS R01 DK060838NIDDK NIH HHS R01 DK060839NIDDK NIH HHS R01 DK080756PHS HHS D57521PHS HHS R37 49132
6 · The paper itself

Abstract

Obesity and type 2 diabetes are characterized by insulin resistance. Mice lacking the protein-tyrosine phosphatase PTP1B in all tissues are hypersensitive to insulin but also have diminished fat stores. Because adiposity affects insulin sensitivity, the extent to which PTP1B directly regulates glucose homeostasis has been unclear. We report that mice lacking PTP1B only in muscle have body weight and adiposity comparable to those of controls on either chow or a high-fat diet (HFD). Muscle triglycerides and serum adipokines are also affected similarly by HFD in both groups. Nevertheless, muscle-specific PTP1B(-/-) mice exhibit increased muscle glucose uptake, improved systemic insulin sensitivity, and enhanced glucose tolerance. These findings correlate with and are most likely caused by increased phosphorylation of the insulin receptor and its downstream signaling components. Thus, muscle PTP1B plays a major role in regulating insulin action and glucose homeostasis, independent of adiposity. In addition, rosiglitazone treatment of HFD-fed control and muscle-specific PTP1B(-/-) mice revealed that rosiglitazone acts additively with PTP1B deletion. Therefore, combining PTP1B inhibition with thiazolidinediones should be more effective than either alone for treating insulin-resistant states.

Indexed as

Gene DeletionHomeostasisAdiposityAnimalsBody WeightCreatine KinaseGlucoseInsulinMiceMice, KnockoutMuscle, SkeletalOrgan SpecificityProtein Tyrosine Phosphatase, Non-Receptor Type 1RosiglitazoneSignal TransductionThiazolidinedionesCreatine KinaseGlucoseInsulinProtein Tyrosine Phosphatase, Non-Receptor Type 1RosiglitazoneThiazolidinedionesTriglycerides

Identifiers

PMID17724080
PMCPMC2169063

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.