Evidence map›Paper›PMID 38190531›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

CLCF1 inhibits energy expenditure via suppressing brown fat thermogenesis.

Youwen Yuan, Kangli Li, Xueru Ye, Shiyi Wen, Yanan Zhang, Fei Teng, Xuan Zhou, Yajuan Deng, Xiaoyu Yang, Weiwei Wang and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

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  12. CLCF1 inhibits energy expenditure via suppressing brown fat thermogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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

15 authors at 3 institutions in 1 country.

Youwen Yuan *Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.ORCID 0000-0002-0159-2146
Kangli Li *Department of Endocrinology, Translational Research of Diabetes Key Laboratory of Chongqing Education Commission of China, The Second Affiliated Hospital of Army Medical University, Chongqing 400037, China.
Xueru Ye *Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Shiyi Wen *Department of Endocrinology and Metabolism, Medical Center for Comprehensive Weight Control, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.ORCID 0009-0007-9825-6432
Yanan ZhangDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Fei TengDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Xuan ZhouDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Yajuan DengDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Xiaoyu YangDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Weiwei WangDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Jiayang LinDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.ORCID 0000-0001-9887-976X
Shenjian LuoDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Peizhen ZhangDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Guojun ShiDepartment of Endocrinology and Metabolism, Medical Center for Comprehensive Weight Control, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.ORCID 0000-0002-3098-6662
Huijie ZhangDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.ORCID 0000-0003-0640-0315
Nanfang Hospital · CNSun Yat-sen University · CNArmy Medical University · CN

Funding

GDSTC | Basic and Applied Basic Research Foundation of Guangdong Province () 2023A1515012202Guangzhou Science and Technology Plan Project 202201020497Guangzhou Science and Technology Plan Project SL2024B03J00202Joint Funds of the National Natural Science Foundation of China U22A20288Key-Area Clinical Research Program of Southern Medical University LC2019ZD010MOST | National Key Research and Development Program of China (NKPs) 2018YFA0800404MOST | National Natural Science Foundation of China (NSFC) 81970736MOST | National Natural Science Foundation of China (NSFC) 82070811MOST | National Natural Science Foundation of China (NSFC) 82300974MOST | NSFC | National Science Fund for Distinguished Young Scholars (National Science Foundation for Distinguished Young Scholars) 82325011
6 · The paper itself

Abstract

Brown adipose tissue (BAT) is the main site of nonshivering thermogenesis which plays an important role in thermogenesis and energy metabolism. However, the regulatory factors that inhibit BAT activity remain largely unknown. Here, cardiotrophin-like cytokine factor 1 (CLCF1) is identified as a negative regulator of thermogenesis in BAT. Adenovirus-mediated overexpression of CLCF1 in BAT greatly impairs the thermogenic capacity of BAT and reduces the metabolic rate. Consistently, BAT-specific ablation of CLCF1 enhances the BAT function and energy expenditure under both thermoneutral and cold conditions. Mechanistically, adenylate cyclase 3 (ADCY3) is identified as a downstream target of CLCF1 to mediate its role in regulating thermogenesis. Furthermore, CLCF1 is identified to negatively regulate the PERK-ATF4 signaling axis to modulate the transcriptional activity of ADCY3, which activates the PKA substrate phosphorylation. Moreover, CLCF1 deletion in BAT protects the mice against diet-induced obesity by promoting BAT activation and further attenuating impaired glucose and lipid metabolism. Therefore, our results reveal the essential role of CLCF1 in regulating BAT thermogenesis and suggest that inhibiting CLCF1 signaling might be a potential therapeutic strategy for improving obesity-related metabolic disorders.

Indexed as

Adipose Tissue, BrownEnergy MetabolismAdenoviridaeAnimalsCytokinesInterleukinsMiceObesityThermogenesisCytokinesInterleukinsnovel neurotrophin-1, mousebrown adipose tissueCLCF1obesitythermogenesis

Identifiers

PMID38190531
PMCPMC10801846
OpenAlexW4390659029

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.