Evidence map›Paper›PMID 32580141›Full record

ArticleEBioMedicine2020

Thrombospondin 1 improves hepatic steatosis in diet-induced insulin-resistant mice and is associated with hepatic fat content in humans.

Jinyun Bai, Mingfeng Xia, Yaqian Xue, Fengguang Ma, Aoyuan Cui, Yixuan Sun, Yamei Han, Xi Xu, Feifei Zhang, Zhimin Hu and 14 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Transcriptome screening and functional validation of FN1 in the regulation of granulosa cell proliferation in polycystic ovary syndrome.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  3. Article
  4. Renal IGFBP6 Interacts With THBS1 to Drive Renal Cellular Senescence and Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors at 7 institutions in 1 country.

Jinyun BaiDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China; Fudan Institute for Metabolic Diseases, Shanghai, China.
Mingfeng XiaDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China; Fudan Institute for Metabolic Diseases, Shanghai, China.
Yaqian XueCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Fengguang MaCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Aoyuan CuiCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Yixuan SunDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China; Fudan Institute for Metabolic Diseases, Shanghai, China.
Yamei HanCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Xi XuDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China; Fudan Institute for Metabolic Diseases, Shanghai, China.
Feifei ZhangCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Zhimin HuCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Zhengshuai LiuCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Yuxiao LiuCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Genxiang CaiCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Weitong SuCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Xiaoyang SunDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China; Fudan Institute for Metabolic Diseases, Shanghai, China.
Haifu WuMetabolic and Bariatric Surgery of Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Hongmei YanDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China; Fudan Institute for Metabolic Diseases, Shanghai, China.
Xinxia ChangDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China; Fudan Institute for Metabolic Diseases, Shanghai, China.
Xiqi HuDepartment of Pathology, Medical College, Fudan University, Shanghai, China.
Hua BianDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China; Fudan Institute for Metabolic Diseases, Shanghai, China.
Pu XiaDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China; Fudan Institute for Metabolic Diseases, Shanghai, China.
Jing GaoCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Yu LiCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. Electronic address: liyu@sibs.ac.cn.
Xin GaoDepartment of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China; Fudan Institute for Metabolic Diseases, Shanghai, China. Electronic address: happy20061208@126.com.
Shanghai Institute of Nutrition and Health · CNZhongshan Hospital · CNShanghai Institutes for Biological Sciences · CNFudan University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNShanghai Medical College of Fudan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNonalcoholic fatty liver disease (NAFLD) is associated with altered production of secreted proteins. Increased understanding of secreted proteins could lead to improved prediction and treatment of NAFLD. Here, we aimed to discover novel secreted proteins in humans that are associated with hepatic fat content using unbiased proteomic profiling strategy, and how the identified Thbs1 modulates lipid metabolism and hepatic steatosis.

methodNAFLD patients were enrolled and treated with lifestyle intervention. Patients who underwent liver biopsy were enrolled for analyzing the correlation between circulating Thbs1 and liver steatosis. Mice were fed on high-fat, high-sucrose diet and treated with recombinant Thbs1. Primary hepatocytes isolated from CD36 knockout (CD36-/-) mice and their wild-type littermates (controls) were treated with glucose plus insulin for 24 h together with or without recombinant Thbs1. FINDING: Serum Thbs1 levels are increased in participants with NAFLD and positively associated with liver steatosis grades. Improvement of liver steatosis after lifestyle intervention was accompanied with significant reduction of serum Thbs1 levels. Pharmacological administration of recombinant human Thbs1 attenuates hepatic steatosis in diet-induced obese mice. Treatment with Thbs1 protein or stably overexpression of Thbs1 causes a significant reduction of lipid accumulation in primary hepatocytes or HepG2 cells exposed to high glucose plus insulin, suggesting that Thbs1 regulates lipid metabolism in a hepatocyte-autonomous manner. Mechanistically, Thbs1 inhibits cleavage and processing of SREBP-1, leading to a reduction of target lipogenic gene expression and hepatic steatosis. Inhibitory effects of Thbs1 on lipogenesis and triglyceride accumulation are abrogated in CD36 deficient primary hepatocytes exposed to high glucose plus insulin. Interestingly, beneficial effects of Thbs1 on lipid accumulation are observed in primary hepatocytes treated with a Thbs1 nonapeptide mimetic ABT-526.

interpretationThbs1 is a biomarker for NAFLD in humans, and pharmacological and genetic approaches for the modulation of Thbs1 activity may have the therapeutic potential for treating hepatic steatosis. FUND: A full list of funding bodies that contributed to this study can be found in the Funding Sources section.

Indexed as

ProteomicsAnimalsCD36 AntigensDiet, High-FatFatty LiverHepatocytesHep G2 CellsHumansInsulinInsulin ResistanceLipid MetabolismLipogenesisLiverMiceMice, KnockoutNon-alcoholic Fatty Liver Diseaseacetyl-sarcosyl-glycyl-valyl-isoleucyl-threonyl-norvalyl-isoleucyl-arginyl-proline ethylamideCD36 AntigensInsulinPeptide FragmentsThrombospondin 1TriglyceridesCD36Hepatic steatosisNAFLDProteomicsThrombospondin 1

Identifiers

PMID32580141
PMCPMC7317187
OpenAlexW3036209699

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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.