Evidence map›Paper›PMID 27163748›Full record

ArticleInternational journal of obesity (2005)2016

Cathelicidin suppresses lipid accumulation and hepatic steatosis by inhibition of the CD36 receptor.

D Hoang-Yen Tran, D Hoang-Ngoc Tran, S A Mattai, T Sallam, C Ortiz, E C Lee, L Robbins, S Ho, J E Lee, E Fisseha and 16 more

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

Article in International journal of obesity (2005), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Neutrophil-T cell cross talk in noninfectious liver diseases.American journal of physiology. Gastrointestinal and liver physiology · 2026
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  12. The Role of Obesity in the Immunopathogenesis of COVID-19 Respiratory Disease and Critical Illness.American journal of respiratory cell and molecular biology · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Article
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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

26 authors at 3 institutions in 1 country.

D Hoang-Yen TranDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
D Hoang-Ngoc TranDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
S A MattaiDepartment of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
T SallamDepartment of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
C OrtizDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
E C LeeDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
L RobbinsDepartment of Medicine, Cedars-Sinai Medical Center, F. Widjaja Foundation, Inflammatory Bowel & Immunobiology Research Institute, Los Angeles, CA, USA.
S HoDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
J E LeeDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
E FissehaDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
C ShiehDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
A SideriDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
D Q ShihDepartment of Medicine, Cedars-Sinai Medical Center, F. Widjaja Foundation, Inflammatory Bowel & Immunobiology Research Institute, Los Angeles, CA, USA.
P FleshnerDepartment of Medicine, Cedars-Sinai Medical Center, F. Widjaja Foundation, Inflammatory Bowel & Immunobiology Research Institute, Los Angeles, CA, USA.
D P B McGovernDepartment of Medicine, Cedars-Sinai Medical Center, F. Widjaja Foundation, Inflammatory Bowel & Immunobiology Research Institute, Los Angeles, CA, USA.
M VuDepartment of Medicine, Cedars-Sinai Medical Center, F. Widjaja Foundation, Inflammatory Bowel & Immunobiology Research Institute, Los Angeles, CA, USA.
T C HingDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
K BakirtziDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
M ChengDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
B SuDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
I LawDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
I KaragiannidesDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
S R TarganDepartment of Medicine, Cedars-Sinai Medical Center, F. Widjaja Foundation, Inflammatory Bowel & Immunobiology Research Institute, Los Angeles, CA, USA.
R L GalloDivision of Dermatology, Department of Medicine, the University of California San Diego, San Diego, CA, USA.
Z LiDivision of Clinical Nutrition, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
H W KoonDivision of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
University of California, Los Angeles · USCedars-Sinai Medical Center · USUniversity of California, San Diego · US

Funding

Using polygenic scores to enhance both variant discovery, and understanding of functional consequences of genetic variation in IBD.P01DK046763 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI TARGAN, STEPHAN R. · 1992 to 2020
$31.1M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Utilizing the Phenomics of IBD to Enhance Gene DiscoveryU01DK062413 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI Dermot Patrick McGovern · 2002 to 2026
$12.2M
Characterizing the gut microbial ecosystem for diagnosis and therapy in IBDU54DE023798 · NIDCR · BROAD INSTITUTE, INC. · PI HUTTENHOWER, CURTIS, XAVIER, RAMNIK J · 2013 to 2014
$3.0M
Role of Cathelicidin in Intestinal InflammationK01DK084256 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KOON, HON WAI · 2010 to 2014
$743k
Role of Cathelicidin in Obesity and DiabetesR03DK103964 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KOON, HON WAI · 2015 to 2016
$154k
NIDCR NIH HHS U54 DE023798NIDDK NIH HHS K01 DK084256NIDDK NIH HHS P01 DK046763NIDDK NIH HHS P30 DK041301NIDDK NIH HHS R03 DK103964NIDDK NIH HHS U01 DK062413
6 · The paper itself

Abstract

BACKGROUND AND

objectivesObesity is a global epidemic which increases the risk of the metabolic syndrome. Cathelicidin (LL-37 and mCRAMP) is an antimicrobial peptide with an unknown role in obesity. We hypothesize that cathelicidin expression correlates with obesity and modulates fat mass and hepatic steatosis. MATERIALS AND

methodsMale C57BL/6 J mice were fed a high-fat diet. Streptozotocin was injected into mice to induce diabetes. Experimental groups were injected with cathelicidin and CD36 overexpressing lentiviruses. Human mesenteric fat adipocytes, mouse 3T3-L1 differentiated adipocytes and human HepG2 hepatocytes were used in the in vitro experiments. Cathelicidin levels in non-diabetic, prediabetic and type II diabetic patients were measured by enzyme-linked immunosorbent assay.

resultsLentiviral cathelicidin overexpression reduced hepatic steatosis and decreased the fat mass of high-fat diet-treated diabetic mice. Cathelicidin overexpression reduced mesenteric fat and hepatic fatty acid translocase (CD36) expression that was reversed by lentiviral CD36 overexpression. Exposure of adipocytes and hepatocytes to cathelicidin significantly inhibited CD36 expression and reduced lipid accumulation. Serum cathelicidin protein levels were significantly increased in non-diabetic and prediabetic patients with obesity, compared with non-diabetic patients with normal body mass index (BMI) values. Prediabetic patients had lower serum cathelicidin protein levels than non-diabetic subjects.

conclusionsCathelicidin inhibits the CD36 fat receptor and lipid accumulation in adipocytes and hepatocytes, leading to a reduction of fat mass and hepatic steatosis in vivo. Circulating cathelicidin levels are associated with increased BMI. Our results demonstrate that cathelicidin modulates the development of obesity.

Indexed as

3T3-L1 CellsAdipocytesAnimalsAntimicrobial Cationic PeptidesCathelicidinsCD36 AntigensCell DifferentiationDiabetes Mellitus, ExperimentalDiet, High-FatDisease Models, AnimalFatty LiverGene Expression RegulationHepatocytesHumansImmunohistochemistryLipid MetabolismAntimicrobial Cationic PeptidesCathelicidinsCD36 Antigens

Identifiers

PMID27163748
PMCPMC5014693
OpenAlexW2392871520

What OpenQuestion holds

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LicenceTDM
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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.