Evidence map›Paper›PMID 28570612›Full record

ArticlePloS one2017

Caveolin1 protects against diet induced hepatic lipid accumulation in mice.

Meng Li, Dahua Chen, Haixiu Huang, Jiewei Wang, Xingyong Wan, Chengfu Xu, Chunxiao Li, Han Ma, Chaohui Yu, Youming Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-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

23 citing papers in PubMed, 46 citations in OpenAlex.

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  9. A Review of Defatting Strategies for Non-Alcoholic Fatty Liver Disease.International journal of molecular sciences · 2022
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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

10 authors at 1 institution in 1 country.

Meng LiDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Dahua ChenDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Haixiu HuangDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Jiewei WangDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Xingyong WanDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Chengfu XuDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Chunxiao LiDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Han MaDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Chaohui YuDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Youming LiDepartment of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimCaveolin1 (CAV1) is involved in lipid homeostasis and endocytosis, but little is known about the significance of CAV1 in the pathogenesis and development of nonalcoholic fatty liver disease (NAFLD). This study aimed to determine the role of CAV1 in NAFLD.

methodsExpression of CAV1 in the in vitro and in vivo models of NAFLD was analyzed. The effects of CAV1 knockdown or overexpression on free fatty acid (FFA)-induced lipid accumulation in L02 cells and AML12 cells were determined. CAV1 knockout (CAV1-KO) mice and their wild-type (WT) littermates were subjected to a high fat diet (HFD) for 4 weeks, and the functional consequences of losing the CAV1 gene and its subsequent molecular mechanisms were also examined.

resultsNoticeably, CAV1 expression was markedly reduced in NAFLD. CAV1 knockdown led to the aggravation of steatosis that was induced by FFA in both L02 cells and AML12 cells, while CAV1 overexpression markedly attenuated lipid accumulation in the cells. Consistent with CAV1 repression in the livers of HFD-induced mice, the CAV1-KO mice exhibited more severe hepatic steatosis upon HFD intake. In addition, increased cholesterol levels and elevated transaminases were detected in the plasma of CAV1-KO mice. The protein expression of SREBP1, a key gene involved in lipogenesis, was augmented following CAV1 suppression in FFA-treated hepatocytes and in the livers of HFD-fed CAV1-KO mice.

conclusionsCAV1 serves as an important protective factor in the development of NAFLD by modulating lipid metabolism gene expression.

Indexed as

Diet, High-FatLipid MetabolismAnimalsCaveolin 1Gene SilencingLiverMiceMice, KnockoutNon-alcoholic Fatty Liver DiseaseCaveolin 1

Identifiers

PMID28570612
PMCPMC5453590
OpenAlexW2620606973

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Registered trials

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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.