Previously we showed that fatty liver formation in overfed geese was
accompanied by PI3K-Akt-mTOR pathway activation and changes in plasma
glucose concentrations. Here, we show that glucose acts in goose
hepatocellular lipid metabolism through the PI3K-Akt-mTOR signaling pathway.
We observed that glucose increased lipogenesis, decreased fatty acid
oxidation and increased very low density lipoprotein triglyceride (VLDL-TG)
assembly and secretion. Co-treatment with glucose and inhibitors of the
PI3K-Akt-mTOR pathway (LY294002, rapamycin, NVP-BEZ235) decreased the levels
of factors involved in lipogenesis and increased the levels of factors
involved in fatty acid oxidation and VLDL-TG assembly and secretion. These
findings show that inhibition of the PI3K-Akt-mTOR pathway decreased
glucose-induced lipogenesis, inhibited the downregulation of fatty acid
oxidation by glucose and increased the upregulation of VLDL-TG assembly and
secretion by glucose. The results presented herein provide further support
for the role of the PI3K-Akt-mTOR pathway in lipid metabolism as we showed
that in goose primary hepatocytes, glucose acts through the
PI3K-Akt-mTOR-dependent pathway to stimulate lipid deposition by increasing
lipogenesis and decreasing fatty acid oxidation and VLDL-TG assembly and
secretion.