Evidence map›Paper›PMID 29386390›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Family with sequence similarity 13, member A modulates adipocyte insulin signaling and preserves systemic metabolic homeostasis.

Donytra Arby Wardhana, Koji Ikeda, Agian Jeffilano Barinda, Dhite Bayu Nugroho, Kikid Rucira Qurania, Keiko Yagi, Keishi Miyata, Yuichi Oike, Ken-Ichi Hirata, Noriaki Emoto

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 30 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 3 institutions in 2 countries.

Donytra Arby WardhanaDepartment of Clinical Pharmacy, Kobe Pharmaceutical University, Higashinada, 658-8558 Kobe, Japan.
Koji IkedaDepartment of Clinical Pharmacy, Kobe Pharmaceutical University, Higashinada, 658-8558 Kobe, Japan; ikedak-circ@umin.ac.jp.
Agian Jeffilano BarindaDepartment of Clinical Pharmacy, Kobe Pharmaceutical University, Higashinada, 658-8558 Kobe, Japan.
Dhite Bayu NugrohoDepartment of Clinical Pharmacy, Kobe Pharmaceutical University, Higashinada, 658-8558 Kobe, Japan.ORCID 0000-0003-2483-9970
Kikid Rucira QuraniaDepartment of Clinical Pharmacy, Kobe Pharmaceutical University, Higashinada, 658-8558 Kobe, Japan.
Keiko YagiDepartment of Clinical Pharmacy, Kobe Pharmaceutical University, Higashinada, 658-8558 Kobe, Japan.ORCID 0000-0002-6340-8674
Keishi MiyataDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, 860-8556 Kumamoto, Japan.
Yuichi OikeDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, 860-8556 Kumamoto, Japan.
Ken-Ichi HirataDivision of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Chuo, 6500017 Kobe, Japan.
Noriaki EmotoDepartment of Clinical Pharmacy, Kobe Pharmaceutical University, Higashinada, 658-8558 Kobe, Japan.
Kobe Pharmaceutical University · JPKumamoto University · JPKobe University · JP

Funding

KOMP2-Phase3 Production and Phenotyping by the DTCC Consortium TCP Transfer to UC DavisUM1OD023221 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KC KENT LLOYD · 2016 to 2026
$45.7M
NIH HHS UM1 OD023221
6 · The paper itself

Abstract

Adipose tissue dysfunction is causally implicated in the impaired metabolic homeostasis associated with obesity; however, detailed mechanisms underlying dysregulated adipocyte functions in obesity remain to be elucidated. Here we searched for genes that provide a previously unknown mechanism in adipocyte metabolic functions and identified family with sequence similarity 13, member A (Fam13a) as a factor that modifies insulin signal cascade in adipocytes. Fam13a was highly expressed in adipose tissue, predominantly in mature adipocytes, and its expression was substantially reduced in adipose tissues of obese compared with lean mice. We revealed that Fam13a accentuated insulin signaling by recruiting protein phosphatase 2A with insulin receptor substrate 1 (IRS1), leading to protection of IRS1 from proteasomal degradation. We further demonstrated that genetic loss of Fam13a exacerbated obesity-related metabolic disorders, while targeted activation of Fam13a in adipocytes ameliorated it in association with altered adipose tissue insulin sensitivity in mice. Our data unveiled a previously unknown mechanism in the regulation of adipocyte insulin signaling by Fam13a and identified its significant role in systemic metabolic homeostasis, shedding light on Fam13a as a pharmacotherapeutic target to treat obesity-related metabolic disorders.

Indexed as

Insulin ResistanceAdipocytesAnimalsFemaleGlucoseGTPase-Activating ProteinsHEK293 CellsHomeostasisHumansInsulinInsulin Receptor Substrate ProteinsMaleMetabolic DiseasesMiceMice, Inbred C57BLMice, TransgenicFAM13A protein, humanGlucoseGTPase-Activating ProteinsInsulinInsulin Receptor Substrate Proteinsadipocyteinsulin signalingIRS1metabolic disorderobesity

Identifiers

PMID29386390
PMCPMC5816206
OpenAlexW2791186999

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.