AI Article Synopsis
- Non-alcoholic fatty liver disease is the most common form of chronic liver disease, often linked to obesity and overnutrition.
- Research focused on GPR55, a receptor potentially involved in liver disease, revealing that its activation can lead to lipid buildup in liver cells, but this effect can be blocked by specific antagonists.
- The study suggests that targeting GPR55 could be a promising treatment strategy for managing non-alcoholic fatty liver disease by preventing lipid accumulation.
Article Abstract
Non-alcoholic fatty liver disease is recognized as the leading cause of chronic liver disease. Overnutrition and obesity are associated with hepatic steatosis. G protein-coupled receptor 55 (GPR55) has not been extensively studied in hepatic steatosis, although its endogenous ligands have been implicated in liver disease progression. Therefore, the functions of GPR55 were investigated in Hep3B human hepatoma cells and mice fed high-fat diets. O-1602, the most potent agonist of GPR55, induced lipid accumulation in hepatocytes, which was reversed by treatment with CID16020046, an antagonist of GPR55. O-1602 also induced intracellular calcium rise in Hep3B cells in a GPR55-independent manner. O-1602-induced lipid accumulation was dependent on the PI3 kinase/Akt/SREBP-1c signaling cascade. Furthermore, we found increased levels of lysophosphatidylinositol species of 16:0, 18:0, 18:1, 18:2, 20:1, and 20:2 in the livers of mice fed a high-fat diet for 4 weeks. One-week treatment with CID16020046 suppressed high-fat diet-induced lipid accumulation and O-1602-induced increase of serum triglyceride levels in vivo. Therefore, the present data suggest the pro-steatotic function of GPR55 signaling in hepatocytes and provide a potential therapeutic target for non-alcoholic fatty liver disease.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8003045 | PMC |
| http://dx.doi.org/10.3390/ijms22063091 | DOI Listing |
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