2016
DOI: 10.18632/aging.101067
View full text |Buy / Rent full text
|
Sign up to set email alerts
|

Abstract: The increased expression of PNPLA3148M leads to hepatosteatosis in mice. This study aims to investigate the genetic control of hepatic PNPLA3 transcription and to explore its impact on NAFLD risk in humans. Through a locus-wide expression quantitative trait loci (eQTL) mapping in two human liver sample sets, a PNPLA3 intronic SNP, rs139051 A>G was identified as a significant eQTL (p = 6.6×10−8) influencing PNPLA3 transcription, with the A allele significantly associated with increased PNPLA3 mRNA. An electroph… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

0
8
0

Year Published

2019
2019
2021
2021

Publication Types

Select...
2
2

Relationship

1
3

Authors

Journals

citations
Cited by 10 publications
(8 citation statements)
references
References 48 publications
(67 reference statements)
0
8
0
Order By: Relevance
“…First, we confirmed that the rs738409 genotype does not impact on PNPLA3 transcript expression, as previously reported by eQTL mapping. 9,15 Secondly, our study suggests an inverse relationship between NAFLD disease activity and PNPLA3 transcription on multiple levels. The PNPLA3 transcript abundance was the lowest in zone 1 hepatocytes where steatosis is the most severe.…”
Section: Discussionmentioning
confidence: 63%
See 1 more Smart Citation
“…First, we confirmed that the rs738409 genotype does not impact on PNPLA3 transcript expression, as previously reported by eQTL mapping. 9,15 Secondly, our study suggests an inverse relationship between NAFLD disease activity and PNPLA3 transcription on multiple levels. The PNPLA3 transcript abundance was the lowest in zone 1 hepatocytes where steatosis is the most severe.…”
Section: Discussionmentioning
confidence: 63%
“…Previous locus-wide expression quantitative trait loci (eQTL) mapping indicates that rs738409 does not impact PNPLA3 transcription. 15 Herein, we aim to examine PNPLA3 transcript levels using quantitative single-cell analysis to determine their relationship with NAFLD disease characteristics.…”
Section: Quantitative Digital Pathology Reveals Association Of Cell-smentioning
confidence: 99%
“…High glucose level can increase the expression of PNPLA3 via regulating carbohydrate-response element-binding protein (ChREBP) 58 , which is a necessary step for the accumulation of PNPLA3-I148M protein on the surface of lipid droplet in hepatocytes. 50,59,60 This accumulation further alters the dynamics of hydrolysis of triglycerides and lead to hepatic steatosis 61 . Therefore, individuals who have a high risk for T2D should consider early intervention to further prevent liver injuries.…”
Section: Discussionmentioning
confidence: 99%
“…He et al 11 found through in vitro experiments that PNPLA3-I148M lost the activity of hydrolyzing triglycerides, causing TGs to accumulate in the liver and gradually form fatty degeneration. In several other studies, it was also found that overexpression of PNPLA3-148M in mice and humans could promote the occurrence of steatosis 45 , 46 . The second mechanism is that PNPLA3-148M will increase the activity of LPAAT to promote the synthesis of TG.…”
Section: Pnpla3 and Liver Diseasementioning
confidence: 81%