Evidence map›Paper›PMID 32733043›Full record

ArticleScientific reports2020

Elafin inhibits obesity, hyperglycemia, and liver steatosis in high-fat diet-treated male mice.

Jiani Wang, Christina Ortiz, Lindsey Fontenot, Riya Mukhopadhyay, Ying Xie, Ivy Ka Man Law, David Q Shih, S Anjani Mattai, Zhaoping Li, Hon Wai Koon

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

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

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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

10 authors at 5 institutions in 2 countries.

Jiani WangVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Room 44-129, Center for Health Sciences Building, 10833 Le Conte Avenue, Los Angeles, CA, 90095, USA.
Christina OrtizVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Room 44-129, Center for Health Sciences Building, 10833 Le Conte Avenue, Los Angeles, CA, 90095, USA.
Lindsey FontenotVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Room 44-129, Center for Health Sciences Building, 10833 Le Conte Avenue, Los Angeles, CA, 90095, USA.
Riya MukhopadhyayVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Room 44-129, Center for Health Sciences Building, 10833 Le Conte Avenue, Los Angeles, CA, 90095, USA.
Ying XieVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Room 44-129, Center for Health Sciences Building, 10833 Le Conte Avenue, Los Angeles, CA, 90095, USA.
Ivy Ka Man LawVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Room 44-129, Center for Health Sciences Building, 10833 Le Conte Avenue, Los Angeles, CA, 90095, USA.
David Q ShihF. Widjaja Foundation, Inflammatory Bowel & Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA.
S Anjani MattaiDepartment of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, 90095, USA.
Zhaoping LiDivision of Clinical Nutrition, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, 90095, USA.
Hon Wai KoonVatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Room 44-129, Center for Health Sciences Building, 10833 Le Conte Avenue, Los Angeles, CA, 90095, USA. hkoon@mednet.ucla.edu.
Oklahoma State University Center for Health Sciences · USUniversity of California, Los Angeles · USCedars-Sinai Medical Center · USChina Medical University · CNFirst Hospital of China Medical University · CN

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
UCLA MSD ProgramR25GM055052 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BARBER, PAUL HENRY, HASSON, TAMA W. · 1996 to 2021
$9.2M
Orally active metabolite therapy against C. difficile infectionR21AI137663 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KOON, HON WAI · 2019 to 2020
$429k
Role of Cathelicidin in Obesity and DiabetesR03DK103964 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KOON, HON WAI · 2015 to 2016
$154k
NIAID NIH HHS AI137663NIAID NIH HHS R21 AI137663NIDDK NIH HHS DK103964NIDDK NIH HHS P30 DK041301NIDDK NIH HHS R03 DK103964NIGMS NIH HHS R25 GM055052
6 · The paper itself

Abstract

Elafin is an antimicrobial and anti-inflammatory protein. We hypothesize that elafin expression correlates with diabetes. Among non-diabetic and prediabetic groups, men have significantly higher serum elafin levels than women. Men with type 2 diabetes mellitus (T2DM) have significantly lower serum elafin levels than men without T2DM. Serum elafin levels are inversely correlated with fasting blood glucose and hemoglobin A1c levels in men with T2DM, but not women with T2DM. Lentiviral elafin overexpression inhibited obesity, hyperglycemia, and liver steatosis in high-fat diet (HFD)-treated male mice. Elafin-overexpressing HFD-treated male mice had increased serum leptin levels, and serum exosomal miR181b-5p and miR219-5p expression. Transplantation of splenocytes and serum exosomes from elafin-overexpressing HFD-treated donor mice reduced food consumption and fat mass, and increased adipose tissue leptin mRNA expression in HFD-treated recipient mice. Elafin improved leptin sensitivity via reduced interferon-gamma expression and induced adipose leptin expression via increased miR181b-5p and miR219-5p expression. Subcutaneous and oral administration of modified elafin inhibited obesity, hyperglycemia, and liver steatosis in the HFD-treated mice. Circulating elafin levels are associated with hyperglycemia in men with T2DM. Elafin, via immune-derived miRNAs and cytokine, activates leptin sensitivity and expression that subsequently inhibit food consumption, obesity, hyperglycemia, and liver steatosis in HFD-treated male mice.

Indexed as

Adipose TissueAnimalsCytokinesDiet, High-FatDisease Models, AnimalEatingElafinFatty LiverFemaleGene ExpressionHumansHyperglycemiaInterferon-gammaLeptinMaleMice, Inbred C57BLCytokinesElafinInterferon-gammaLeptin

Identifiers

PMID32733043
PMCPMC7393145
OpenAlexW3046028705

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.