Evidence map›Paper›PMID 28515350›Full record

ArticleOncotarget2017

FAM3A enhances adipogenesis of 3T3-L1 preadipocytes via activation of ATP-P2 receptor-Akt signaling pathway.

Yujing Chi, Jing Li, Na Li, Zhenzhen Chen, Liping Ma, Weikang Peng, Xiuying Pan, Mei Li, Weidong Yu, Xiangjun He and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Intracellular ATP Signaling Contributes to FAM3A-Induced PDX1 Upregulation in Pancreatic Beta Cells.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2022
    Article
  6. Review
  7. Review
  8. Article
  9. Novel Targets for Treating Ischemia-Reperfusion Injury in the Liver.International journal of molecular sciences · 2018
    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

14 authors at 2 institutions in 1 country.

Yujing ChiInstitute of Clinical Molecular Biology & Central Laboratory, Peking University People's Hospital, Beijing 100044, China.
Jing LiDepartment of Gastroenterology, Peking University People's Hospital, Beijing 100044, China.
Na LiInstitute of Clinical Molecular Biology & Central Laboratory, Peking University People's Hospital, Beijing 100044, China.
Zhenzhen ChenDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, Key Laboratory of Cardiovascular Science of the Ministry of Education, Center for Non-coding RNA Medicine, Beijing 100191, China.
Liping MaInstitute of Clinical Molecular Biology & Central Laboratory, Peking University People's Hospital, Beijing 100044, China.
Weikang PengInstitute of Clinical Molecular Biology & Central Laboratory, Peking University People's Hospital, Beijing 100044, China.
Xiuying PanInstitute of Clinical Molecular Biology & Central Laboratory, Peking University People's Hospital, Beijing 100044, China.
Mei LiInstitute of Clinical Molecular Biology & Central Laboratory, Peking University People's Hospital, Beijing 100044, China.
Weidong YuInstitute of Clinical Molecular Biology & Central Laboratory, Peking University People's Hospital, Beijing 100044, China.
Xiangjun HeInstitute of Clinical Molecular Biology & Central Laboratory, Peking University People's Hospital, Beijing 100044, China.
Bin GengDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, Key Laboratory of Cardiovascular Science of the Ministry of Education, Center for Non-coding RNA Medicine, Beijing 100191, China.
Qinghua CuiDepartment of Biomedical Informatics, School of Basic Medical Sciences, Peking University Health Science Center, Key Laboratory of Cardiovascular Science of the Ministry of Education, Center for Non-coding RNA Medicine, Beijing 100191, China.
Yulan LiuInstitute of Clinical Molecular Biology & Central Laboratory, Peking University People's Hospital, Beijing 100044, China.
Jichun YangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, Key Laboratory of Cardiovascular Science of the Ministry of Education, Center for Non-coding RNA Medicine, Beijing 100191, China.
Peking University · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FAM3A plays important roles in regulating hepatic glucose/lipid metabolism and the proliferation of VSMCs. This study determined the role and mechanism of FAM3A in the adipogenesis of 3T3-L1 preadipocytes. During the adipogenesis of 3T3-L1 preadipocytes, FAM3A expression was significantly increased. FAM3A overexpression enhanced 3T3-L1 preadipocyte adipogenesis with increased phosphorylated Akt (pAkt) level, whereas FAM3A silencing inhibited 3T3-L1 preadipocyte adipogenesis with reduced pAkt level. Moreover, FAM3A silencing reduced the expression and secretion of adipokines in 3T3-L1 cells. FAM3A protein is mainly located in mitochondrial fraction of 3T3-L1 cells and mouse adipose tissue. FAM3A overexpression increased, whereas FAM3A silencing decreased ATP production in 3T3-L1 preadipocytes. FAM3A-induced adipogenesis of 3T3-L1 preadipocytes was blunted by inhibitor of P2 receptor. In white adipose tissues of db/db and HFD-fed obese mice, FAM3A expression was reduced. One-month rosiglitazone administration upregulated FAM3A expression, and increased cellular ATP content and pAkt level in white adipose tissues of normal and obese mice. In conclusion, FAM3A enhances the adipogenesis of preadipocytes by activating ATP-P2 receptor-Akt pathway. Under obese condition, a decrease in FAM3A expression in adipose tissues plays important roles in the development of adipose dysfunction and type 2 diabetes.

Indexed as

AdipogenesisSignal Transduction3T3-L1 CellsAdenosine TriphosphateAdipocytesAdipose Tissue, WhiteAnimalsCell DifferentiationCytokinesGene Expression RegulationGene SilencingMaleMicePPAR gammaProto-Oncogene Proteins c-aktReceptors, Purinergic P2Adenosine TriphosphateCytokinesFAM3A protein, mousePPAR gammaProto-Oncogene Proteins c-aktReceptors, Purinergic P2RosiglitazoneThiazolidinedionesadipogenesisATPFAM3AP2 receptorPPARγ

Identifiers

PMID28515350
PMCPMC5542233
OpenAlexW2610241526

What OpenQuestion holds

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LicenceCC BY
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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.