Evidence map›Paper›PMID 25972571›Full record

ArticleDiabetes2015

Forced Hepatic Overexpression of CEACAM1 Curtails Diet-Induced Insulin Resistance.

Qusai Y Al-Share, Anthony M DeAngelis, Sumona Ghosh Lester, Thomas A Bowman, Sadeesh K Ramakrishnan, Simon L Abdallah, Lucia Russo, Payal R Patel, Meenakshi K Kaw, Christian K Raphael and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  13. Insulin Clearance in Obesity and Type 2 Diabetes.International journal of molecular sciences · 2022
    Review
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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

17 authors at 4 institutions in 1 country.

Qusai Y Al-ShareCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH.
Anthony M DeAngelisCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH.
Sumona Ghosh LesterCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH.
Thomas A BowmanCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH.
Sadeesh K RamakrishnanCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH.
Simon L AbdallahCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH.
Lucia RussoCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH.
Payal R PatelCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH.
Meenakshi K KawCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH.
Christian K RaphaelCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH.
Andrea Jung KimCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Rehabilitation Sciences, College of Health Sciences, The University of Toledo, Toledo, OH.
Garrett HeinrichCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Rehabilitation Sciences, College of Health Sciences, The University of Toledo, Toledo, OH.
Abraham D LeeCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Rehabilitation Sciences, College of Health Sciences, The University of Toledo, Toledo, OH.
Jason K KimProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA.
Rohit N KulkarniResearch Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA.
William M PhilbrickSection of Endocrinology and Metabolism, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT.
Sonia M NajjarCenter for Diabetes and Endocrine Research, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH sonia.najjar@utoledo.edu.
University of Toledo · USJoslin Diabetes Center · USUniversity of Massachusetts Chan Medical School · USYale University · US

Funding

Role of IGF-1 and Insulin Receptors Beta-Cell SurvivalR01DK067536 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 2004 to 2026
$8.0M
SUBSTRATES AND INSULIN RECEPTOR ENDOCYTOSISR01DK054254 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI NAJJAR, SONIA M. · 2000 to 2021
$5.8M
Role of SerpinB1 in beta cell growthR01DK103215 · NIDDK · JOSLIN DIABETES CENTER · PI KULKARNI, ROHIT N. · 2014 to 2018
$2.6M
UMass Mouse Metabolic Phenotyping CenterU24DK093000 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KIM, JASON K · 2011 to 2015
$2.1M
CEACAM1: A link between metabolic and cardiovascular diseasesR01HL112248 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI NAJJAR, SONIA M. · 2012 to 2016
$1.9M
Insulin resistance in the pathogenesis of NASHR01DK083850 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI NAJJAR, SONIA M. · 2009 to 2010
$749k
NHLBI NIH HHS R01 HL112248NHLBI NIH HHS R01-HL-112248NIDDK NIH HHS R01 DK054254NIDDK NIH HHS R01-DK-054254NIDDK NIH HHS R01 DK067536NIDDK NIH HHS R01 DK083850NIDDK NIH HHS R01-DK-083850NIDDK NIH HHS R01 DK103215NIDDK NIH HHS R01-DK-103215NIDDK NIH HHS R01-DK-67536NIDDK NIH HHS U24 DK093000NIDDK NIH HHS U24-DK-093000
6 · The paper itself

Abstract

Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) regulates insulin sensitivity by promoting hepatic insulin clearance. Liver-specific inactivation or global null-mutation of Ceacam1 impairs hepatic insulin extraction to cause chronic hyperinsulinemia, resulting in insulin resistance and visceral obesity. In this study we investigated whether diet-induced insulin resistance implicates changes in hepatic CEACAM1. We report that feeding C57/BL6J mice a high-fat diet reduced hepatic CEACAM1 levels by >50% beginning at 21 days, causing hyperinsulinemia, insulin resistance, and elevation in hepatic triacylglycerol content. Conversely, liver-specific inducible CEACAM1 expression prevented hyperinsulinemia and markedly limited insulin resistance and hepatic lipid accumulation that were induced by prolonged high-fat intake. This was partly mediated by increased hepatic β-fatty acid oxidation and energy expenditure. The data demonstrate that the high-fat diet reduced hepatic CEACAM1 expression and that overexpressing CEACAM1 in liver curtailed diet-induced metabolic abnormalities by protecting hepatic insulin clearance.

Indexed as

Diet, High-FatAnimalsAntigens, CDCell Adhesion MoleculesEnergy MetabolismFatty AcidsHyperinsulinismInsulinInsulin ResistanceLiverMiceMice, TransgenicAntigens, CDCD66 antigensCell Adhesion MoleculesFatty AcidsInsulin

Identifiers

PMID25972571
PMCPMC4512217
OpenAlexW2212750191

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.