Abstract

In this study, we investigated the role of liver X receptor (LXR) activation in hepatic assembly and in the secretion of very low density lipoprotein-triglycerides in goose primary hepatocytes. Goose primary hepatocytes were isolated and treated with the LXR agonist T0901317. Total triglyceride accumulation, intracellular and extracellular triglyceride concentrations, extracellular very low density lipoprotein concentration, and gene expression levels of LXRα, microsomal triglyceride transfer protein, acyl coenzyme A:diacylglycerol acyltransferase (DGAT) 1, and DGAT2 were measured in primary hepatocytes. We found a dose-dependent upregulation of total and intracellular TG accumulation when using 0, 0.01, 0.1, 1, and 10 μM T0901317, but the extracellular triglyceride and very low density lipoprotein concentrations were dose dependent only when the T0901317 concentration was below 1 μM; as compared with 1 μM T0901317, 10 μM T0901317 had an inhibiting effect (P < 0.05). The mRNA levels of all the detected genes increased in the presence of T0901317. The change in LXRα and DGAT1 was dose dependent, and the mRNA levels of microsomal triglyceride transfer protein and DGAT2 increased with a T0901317 concentration up to 1 μM, but decreased when treated with 10 μM T0901317 (P < 0.05). In conclusion, the secretion of very low density lipoprotein plays a role in pharmacologically activating the LXR-induced development of hepatocellular steatosis in geese.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call