Evidence map›Paper›PMID 32862405›Full record

ArticleEndocrine2020

PNPLA3 I148M is involved in the variability in anti-NAFLD response to exenatide.

Yunzhi Chen, Xuemei Yan, Xiao Xu, Shuhua Yuan, Fen Xu, Hua Liang

Abstract read
PubMed Publisher
In one paragraph

Article in Endocrine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Liver Fat Changes in Patients With Type 2 Diabetes by Presence of Genetic Hepatic Steatosis: A Post Hoc Analysis of SURPASS-3 MRI.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
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

6 authors at 3 institutions in 1 country.

Yunzhi Chen *Department of Endocrinology and Metabolism, Third Affiliated Hospital of Sun Yat-Sen University, and Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China.
Xuemei Yan *Department of Endocrinology and Metabolism, No. 903 Hospital of PLA Joint Logistic Support Force, Hangzhou, China.
Xiao XuDepartment of Endocrinology and Metabolism, Third Affiliated Hospital of Sun Yat-Sen University, and Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China.
Shuhua YuanDepartment of Endocrinology, Guangzhou Panyu Central Hospital, Guangzhou, China.
Fen XuDepartment of Endocrinology and Metabolism, Third Affiliated Hospital of Sun Yat-Sen University, and Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China.
Hua LiangDepartment of Endocrinology and Metabolism, Third Affiliated Hospital of Sun Yat-Sen University, and Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China. letitia.yw@163.com.
Third Affiliated Hospital of Sun Yat-sen University · CNPanyu District Central Hospital · CNSun Yat-sen University · CN

Funding

lacal innovative and reseach team project of Guangdong Pearl River Talents Program 2017BT01S131National Natural Science Foundation of China 81370909Natural Science Foundation of Guangdong Province 2020A1515010226
6 · The paper itself

Abstract

purposeGLP-1 receptor agonists, such as exenatide, have been proven to attenuate nonalcoholic fatty liver disease (NAFLD) in vivo and in vitro. However, the efficiency of exenatide had interindividual differences. PNPLA3 is a major susceptibility gene for NAFLD and its I148M polymorphism increases the risk of all disorders of the NAFLD spectrum. Whether this variant contributes to variability in exenatide response is still unclear.

methodsPNPLA3 148I knockin HepG2 cells were constructed using the Cas9/sgRNA system. Oil Red O staining combined with TG quantification was used to evaluate lipid accumulation. Western blotting and qRT-qPCR were conducted, respectively, to measure the protein and mRNA expression of lipid metabolic and endoplasmic reticulum (ER) stress-related inflammatory markers. PNPLA3 I148M was genotyped in type 2 diabetics using Sanger sequencing. The exenatide-induced changes in liver fat content and other clinical parameters were compared between PNPLA3 I148M genotypes.

resultsLipid deposition increased in both PNPLA3 148I/I and 148M/M HepG2 cells treated with palmitoleic acid, while cells with 148M/M had a higher TG content than those with 148I/I. Exendin-4 treatment was showed to be more significant in 148I/I cells than in 148M/M cells in terms of reducing the intrahepatic fat content, inhibiting SREBP-1c and ER stress-related inflammation, and activating AMPK-ACC lipid oxidation pathway. In patients with type 2 diabetes, 24-week treatment with exenatide improved liver fat content in patients carrying PNPLA3 148I/I better than in patients with 148M/M.

conclusionsPNPLA3 I148M might modify the anti-NAFLD response to exenatide.

Indexed as

Diabetes Mellitus, Type 2Non-alcoholic Fatty Liver DiseaseAcyltransferasesExenatideGenetic Predisposition to DiseaseGenotypeHep G2 CellsHumansLipaseLiverMembrane ProteinsPhospholipases A2, Calcium-IndependentAcyltransferasesExenatideLipaseMembrane ProteinsPhospholipases A2, Calcium-IndependentPNPLA3 protein, humanGLP-1 receptor agonistLiver fat contentNAFLDPNPLA3 I148MType 2 diabetes

Identifiers

PMID32862405
OpenAlexW3082644014

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.