ArticlePhytotherapy research : PTR2026
Liquiritigenin Ameliorates High-Fat Diet-Induced Hepatic Steatosis by Promoting Lipid Droplet Catabolism via PLIN2-ATGL Regulation.
Article in Phytotherapy research : PTR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Metabolic-associated fatty liver disease (MAFLD), formerly known as non-alcoholic fatty liver disease (NAFLD) has caused a significant health burden. Glycyrrhiza uralensis Fisch. is a traditional Chinese medicinal herb used to prevent and treat numerous diseases. Liquiritigenin (LQ), a flavonoid isolated from Glycyrrhiza uralensis Fisch., has shown potential benefits in regulating lipid metabolism. This study aimed to analyze whether LQ was involved in ameliorating hepatic steatosis and elucidate the specific molecular mechanisms. A high-fat diet (HFD) model of male C57BL/6J mice was established to evaluate the effects of LQ on regulating hepatic steatosis. The potential molecular mechanisms of LQ on promoting lipid droplet catabolism were assessed in vitro using HepG2 cells treated with palmitic acid (PA) and/or LQ. The impact of the PLIN2-ATGL signaling in lipid droplet catabolism was elucidated by treating HepG2 cells with NG-497 (an ATGL inhibitor), the inhibitor of ATGL, and by constructing Plin2-overexpressed HepG2 cell lines. Both in vivo and in vitro experiments demonstrated that LQ alleviated excessive lipid accumulation, enhanced lipolysis and lipophagy, down-regulated PLIN2 expression and up-regulated CGI-58 expression. Further, inhibiting lipolysis with NG-497, the inhibitor of ATGL, attenuated the effects of LQ on increasing the phosphorylation of HSL and promoting lipophagy. The results also showed that transfecting HepG2 cells with a Plin2-overexpressing vector reduced the effects of LQ on up-regulating the expression of CGI-58, as well as proteins related to lipolysis and lipophagy. LQ promoted lipid droplet catabolism through the activation of lipolysis and lipophagy by regulating PLIN2-ATGL signaling, which provided evidence for developing LQ as a functional compound in food for ameliorating hepatic steatosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.