Evidence map›Paper›PMID 26859361›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2016

Hexim1, a Novel Regulator of Leptin Function, Modulates Obesity and Glucose Disposal.

Manya Dhar-Mascareno, Susan N Ramirez, Inna Rozenberg, Yves Rouille, John G Kral, Eduardo J Mascareno

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

Article in Molecular endocrinology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
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

6 authors at 4 institutions in 2 countries.

Manya Dhar-MascarenoDepartment of Biological Sciences (M.D.-M., S.N.R.), State University of New York, College at Old Westbury, Old Westbury, New York 11568; Departments of Cell Biology (I.R., E.J.M.) and Surgery, Medicine, and Cell Biology (J.G.K.), State University of New York Downstate Medical Center, Brooklyn, New York 11203; and Institute Pasteur Inserm (Y.R.), Cenre National de la Recherche Scientifique, Center for Infection and Immunity of Lille, UMR8204, U1019, F-59021 Lille, France.
Susan N RamirezDepartment of Biological Sciences (M.D.-M., S.N.R.), State University of New York, College at Old Westbury, Old Westbury, New York 11568; Departments of Cell Biology (I.R., E.J.M.) and Surgery, Medicine, and Cell Biology (J.G.K.), State University of New York Downstate Medical Center, Brooklyn, New York 11203; and Institute Pasteur Inserm (Y.R.), Cenre National de la Recherche Scientifique, Center for Infection and Immunity of Lille, UMR8204, U1019, F-59021 Lille, France.
Inna RozenbergDepartment of Biological Sciences (M.D.-M., S.N.R.), State University of New York, College at Old Westbury, Old Westbury, New York 11568; Departments of Cell Biology (I.R., E.J.M.) and Surgery, Medicine, and Cell Biology (J.G.K.), State University of New York Downstate Medical Center, Brooklyn, New York 11203; and Institute Pasteur Inserm (Y.R.), Cenre National de la Recherche Scientifique, Center for Infection and Immunity of Lille, UMR8204, U1019, F-59021 Lille, France.
Yves RouilleDepartment of Biological Sciences (M.D.-M., S.N.R.), State University of New York, College at Old Westbury, Old Westbury, New York 11568; Departments of Cell Biology (I.R., E.J.M.) and Surgery, Medicine, and Cell Biology (J.G.K.), State University of New York Downstate Medical Center, Brooklyn, New York 11203; and Institute Pasteur Inserm (Y.R.), Cenre National de la Recherche Scientifique, Center for Infection and Immunity of Lille, UMR8204, U1019, F-59021 Lille, France.
John G KralDepartment of Biological Sciences (M.D.-M., S.N.R.), State University of New York, College at Old Westbury, Old Westbury, New York 11568; Departments of Cell Biology (I.R., E.J.M.) and Surgery, Medicine, and Cell Biology (J.G.K.), State University of New York Downstate Medical Center, Brooklyn, New York 11203; and Institute Pasteur Inserm (Y.R.), Cenre National de la Recherche Scientifique, Center for Infection and Immunity of Lille, UMR8204, U1019, F-59021 Lille, France.
Eduardo J MascarenoDepartment of Biological Sciences (M.D.-M., S.N.R.), State University of New York, College at Old Westbury, Old Westbury, New York 11568; Departments of Cell Biology (I.R., E.J.M.) and Surgery, Medicine, and Cell Biology (J.G.K.), State University of New York Downstate Medical Center, Brooklyn, New York 11203; and Institute Pasteur Inserm (Y.R.), Cenre National de la Recherche Scientifique, Center for Infection and Immunity of Lille, UMR8204, U1019, F-59021 Lille, France.
SUNY Downstate Health Sciences University · USSUNY Old Westbury · USInserm · FRState University of New York · US

Funding

Hexim-1, a novel regulator of prostate cancer progressionR15CA169984 · NCI · COLLEGE AT OLD WESTBURY · PI DHAR-MASCARENO, MANYA · 2012 to 2012
$360k
NCI NIH HHS R15 CA169984NCI NIH HHS R15CA169984
6 · The paper itself

Abstract

Leptin triggers signaling events with significant transcriptional responses that are essential to metabolic processes affecting obesity and glucose disposal. We asked whether hexamethylene bis-acetamide inducible-1 (Hexim1), an inhibitor of RNA II polymerase-dependent transcription elongation, regulates leptin-Janus kinase 2 signaling axis in the hypothalamus. We subjected C57BL6 Hexim1 heterozygous (HT) mice to high-fat diet and when compared with wild type, HT mice were resistant to high-fat diet-induced weight gain and remain insulin sensitive. HT mice exhibited increased leptin-pY(705)Stat3 signaling in the hypothalamus, with normal adipocyte size, increased type I oxidative muscle fiber density, and enhanced glucose transporter 4 expression. We also observed that normal Hexim1 protein level is required to facilitate the expression of CCAAT/enhancer-binding proteins (C/EBPs) required for adipogenesis and inducible suppressor of cytokine signaling 3 (SOCS) expression. Further support on the role of Hexim1 regulating C/EBPs during adipocyte differentiation was shown when HT 3T3L1 fibroblasts failed to undergo adipogenesis. Hexim1 selectively modulates leptin-mediated signal transduction pathways in the hypothalamus, the expression of C/EBPs and peroxisome proliferator-activated receptor-γ (PPAR γ) in skeletal muscle and adipose tissue during the adaptation to metabolic stress. We postulate that Hexim1 might be a novel factor involved in maintaining whole-body energy balance.

Indexed as

3T3 CellsAdipogenesisAnimalsArcuate Nucleus of HypothalamusDiet, High-FatGlucoseGlucose Transporter Type 4HaploinsufficiencyHEK293 CellsHeterozygoteHumansJanus Kinase 2LeptinMaleMiceMice, Inbred C57BLGlucoseGlucose Transporter Type 4Hexim1 protein, mouseJak2 protein, mouseJanus Kinase 2LeptinPhosphotyrosineRNA-Binding ProteinsSlc2a4 protein, mouseSTAT3 Transcription FactorTranscription Factors

Identifiers

PMID26859361
PMCPMC4771697
OpenAlexW2253991585

What OpenQuestion 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 OpenQuestion graph.