Evidence map›Paper›PMID 33743152›Full record

ArticleCell stress & chaperones2021

Heat stress promotes lipid accumulation by inhibiting the AMPK-PGC-1α signaling pathway in 3T3-L1 preadipocytes.

Yanna Huang, Hongyue Xie, Peng Pan, Qiuhong Qu, Qin Xia, Xiaotong Gao, Sanbao Zhang, Qinyang Jiang

Open access · greenAbstract read
In one paragraph

Article in Cell stress & chaperones, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.5field-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

18 citing papers in PubMed, 32 citations in OpenAlex.

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  13. Molecular Mechanism of m6A Methylation Modification GenesInternational journal of molecular sciences · 2023
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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

8 authors at 1 institution in 1 country.

Yanna Huang *College of Animal Science and Technology, Guangxi University, Nanning, 530004, Guangxi, China.
Hongyue Xie *College of Animal Science and Technology, Guangxi University, Nanning, 530004, Guangxi, China.
Peng PanCollege of Animal Science and Technology, Guangxi University, Nanning, 530004, Guangxi, China.
Qiuhong QuCollege of Animal Science and Technology, Guangxi University, Nanning, 530004, Guangxi, China.
Qin XiaCollege of Animal Science and Technology, Guangxi University, Nanning, 530004, Guangxi, China.
Xiaotong GaoCollege of Animal Science and Technology, Guangxi University, Nanning, 530004, Guangxi, China.
Sanbao ZhangCollege of Animal Science and Technology, Guangxi University, Nanning, 530004, Guangxi, China.
Qinyang JiangCollege of Animal Science and Technology, Guangxi University, Nanning, 530004, Guangxi, China. jiangqinyang2013@gxu.edu.cn.ORCID http://orcid.org/0000-0002-0835-9347
Guangxi University · CN

Funding

National Natural Science Foundation of China 31760672 and 31460606
6 · The paper itself

Abstract

Heat stress (HS) results in health problems in animals. This study was conducted to investigate the effect and the underlying mechanism of HS on the proliferation and differentiation process of 3T3-L1 preadipocytes. 3T3-L1 preadipocytes were treated at 37 °C or 41.5 °C. HS up-regulated the mRNA and protein expression level of heat shock protein 70 (HSP70). Furthermore, the proliferation of 3T3-L1 preadipocytes were significantly inhibited after HS treatment for 2 days. A large number of accumulated lipid droplets were observed under the microscope after HS treatment for 8 days. Notably, the result of oil red O staining showed that the number of lipid droplets increased significantly and the differentiation ability of the cells was enhanced after HS. Moreover, after 2 and 8 d of differentiation, HS increased the transcription levels of fat synthesis genes including peroxisome proliferators activated receptor γ (PPARγ), fatty acid binding protein 2 (AP2), fatty acid synthase (FAS) and CCAAT enhancer binding protein α (CEBPα) genes, while decreasing the transcription levels of lipid decomposition genes including ATGL and HSL genes. In addition, HS reduced the expression of AMPK and PGC-1α, as well as the dephosphorylation of AMPK. 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) can eliminate HS induced lipogenesis by activating AMPK. These results indicated that HS inhibited the proliferation of 3T3-L1 preadipocytes and promoted lipid accumulation by inhibiting the AMPK-PGC-1α signaling pathway in 3T3-L1 preadipocytes. This work lays a theoretical foundation for improving the effect of HS on meat quality of livestock and provides a new direction for the prevention of obesity caused by HS.

Indexed as

Hot Temperature3T3-L1 CellsAdipocytesAdipogenesisAMP-Activated Protein KinasesAnimalsMicePPAR gammaSignal TransductionAMP-Activated Protein KinasesPPAR gamma3T3-L1 preadipocyteAMPKDifferentiationHeat stressPGC-1αProliferation

Identifiers

PMID33743152
PMCPMC8065074
OpenAlexW3138291106

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.