Evidence map›Paper›PMID 38168040›Full record

ArticleNature communications2024

Surplus fatty acid synthesis increases oxidative stress in adipocytes and lnduces lipodystrophy.

Li Weng, Wen-Shuai Tang, Xu Wang, Yingyun Gong, Changqin Liu, Ni-Na Hong, Ying Tao, Kuang-Zheng Li, Shu-Ning Liu, Wanzi Jiang and 12 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

24 citing papers in PubMed, 31 citations in OpenAlex.

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  17. Necroptosis in obesity: a complex cell death event.Apoptosis : an international journal on programmed cell death · 2025
    Review
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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

22 authors at 9 institutions in 1 country.

Li Weng *State Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Drug Clinical Trial Center, Shanghai Xuhui Central Hospital / Zhongshan-Xuhui Hospital, Zhongshan Hospital, Fudan University, Shanghai, China.
Wen-Shuai Tang *State Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Drug Clinical Trial Center, Shanghai Xuhui Central Hospital / Zhongshan-Xuhui Hospital, Zhongshan Hospital, Fudan University, Shanghai, China.
Xu Wang *School of Life Science, Anhui Medical University, Research Center for Translational Medicine, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Yingyun Gong *Department of Endocrinology and Metabolism, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID 0000-0002-8570-6904
Changqin LiuDepartment of Endocrinology and Diabetes, the First Affiliated Hospital, Xiamen University, Xiamen, Fujian, China.ORCID 0000-0001-8063-7906
Ni-Na HongState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Ying TaoState Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Drug Clinical Trial Center, Shanghai Xuhui Central Hospital / Zhongshan-Xuhui Hospital, Zhongshan Hospital, Fudan University, Shanghai, China.
Kuang-Zheng LiState Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Drug Clinical Trial Center, Shanghai Xuhui Central Hospital / Zhongshan-Xuhui Hospital, Zhongshan Hospital, Fudan University, Shanghai, China.
Shu-Ning LiuOptogenetics & Synthetic Biology Interdisciplinary Research Center, Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai, China.
Wanzi JiangDepartment of Endocrinology and Metabolism, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Ying LiDepartment of Endocrinology, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China.
Ke YaoSchool of Pharmaceutical Sciences, Tsinghua-Peking Joint Center for Life Sciences, Beijing Frontier Research Center for Biological Structure, Tsinghua University, Beijing, China.ORCID 0000-0003-2638-2978
Li ChenState Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Drug Clinical Trial Center, Shanghai Xuhui Central Hospital / Zhongshan-Xuhui Hospital, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID 0000-0001-8685-3466
He HuangState Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Drug Clinical Trial Center, Shanghai Xuhui Central Hospital / Zhongshan-Xuhui Hospital, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID 0000-0002-2394-0877
Yu-Zheng ZhaoOptogenetics & Synthetic Biology Interdisciplinary Research Center, Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai, China.ORCID 0000-0001-5400-0135
Ze-Ping HuSchool of Pharmaceutical Sciences, Tsinghua-Peking Joint Center for Life Sciences, Beijing Frontier Research Center for Biological Structure, Tsinghua University, Beijing, China.ORCID 0000-0003-4146-7750
Youli LuShanghai Engineering Research Center of Phase I Clinical Research & Quality Consistency Evaluation for Drugs, Institute of Clinical Mass Spectrometry, Shanghai Academy of Experimental Medicine, Shanghai, China.
Haobin YeState Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Drug Clinical Trial Center, Shanghai Xuhui Central Hospital / Zhongshan-Xuhui Hospital, Zhongshan Hospital, Fudan University, Shanghai, China.
Xingrong DuState Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Drug Clinical Trial Center, Shanghai Xuhui Central Hospital / Zhongshan-Xuhui Hospital, Zhongshan Hospital, Fudan University, Shanghai, China.
Hongwen ZhouDepartment of Endocrinology and Metabolism, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. drhongwenzhou@njmu.edu.cn.ORCID 0000-0002-9309-3546
Peng LiState Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Drug Clinical Trial Center, Shanghai Xuhui Central Hospital / Zhongshan-Xuhui Hospital, Zhongshan Hospital, Fudan University, Shanghai, China. li-peng@mail.tsinghua.edu.cn.ORCID 0000-0002-8629-5246
Tong-Jin ZhaoState Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Drug Clinical Trial Center, Shanghai Xuhui Central Hospital / Zhongshan-Xuhui Hospital, Zhongshan Hospital, Fudan University, Shanghai, China. zhaotj@fudan.edu.cn.ORCID 0000-0001-6861-3071
Fudan University · CNJiangsu Province Hospital · CNCenter for Life Sciences · CNEast China University of Science and Technology · CNXiamen University · CNAnhui Medical University · CNFirst Affiliated Hospital of Xiamen University · CNNorthern Jiangsu People's Hospital · CNZhengzhou University of Light Industry · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipocytes are the primary sites for fatty acid storage, but the synthesis rate of fatty acids is very low. The physiological significance of this phenomenon remains unclear. Here, we show that surplus fatty acid synthesis in adipocytes induces necroptosis and lipodystrophy. Transcriptional activation of FASN elevates fatty acid synthesis, but decreases NADPH level and increases ROS production, which ultimately leads to adipocyte necroptosis. We identify MED20, a subunit of the Mediator complex, as a negative regulator of FASN transcription. Adipocyte-specific male Med20 knockout mice progressively develop lipodystrophy, which is reversed by scavenging ROS. Further, in a murine model of HIV-associated lipodystrophy and a human patient with acquired lipodystrophy, ROS neutralization significantly improves metabolic disorders, indicating a causal role of ROS in disease onset. Our study well explains the low fatty acid synthesis rate in adipocytes, and sheds light on the management of acquired lipodystrophy.

Indexed as

AdipocytesLipodystrophyAnimalsFatty AcidsHumansMaleMiceMice, KnockoutOxidative StressReactive Oxygen SpeciesFatty AcidsReactive Oxygen Species

Identifiers

PMID38168040
PMCPMC10761979
OpenAlexW4390506671

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.