Inhibition of PI3K-Akt-mTOR signal pathway dismissed the stimulation of glucose on goose liver cell growth.

Abstract

In the formation of goose fatty liver induced by a high-carbohydrate diet, it is characterized by the quick cell growth of liver. The carbohydrate is mostly digested and absorbed in the small intestine by the form of glucose. Recent studies have suggested a crucial role for PI3K-Akt-mTOR pathway in regulating cell proliferation, and then we speculate that PI3K-Akt-mTOR pathway may mediate glucose-induced liver cell proliferation. Goose primary hepatocytes were isolated and incubated in either no addition as a control or glucose or PI3K-Akt-mTOR pathway inhibitors or cotreatment with glucose and PI3K-Akt-mTOR pathway inhibitors. The results firstly showed that 35mmol/l glucose stimulated the mRNA level and protein content of factors involved in PI3K-Akt-mTOR signal pathway in goose primary hepatocytes. Secondly, 35mmol/l glucose evidently changed the cell cycle PI index and protein expression of cyclin D1. Meanwhile, the upregulation of 35mmol/l glucose on the DNA synthesis rate, cell cycle PI index, the mRNA expression, protein content and protein expression of factors involved in the cell proliferation was decreased significantly by the inhibitors of PI3K-Akt-mTOR pathway, LY294002, rapamycin or NVP-BEZ235. In summary, glucose could stimulate the cell proliferation, and the PI3K-Akt-mTOR pathway inhibitors could dismiss glucose-induced the upregulation of cell proliferation in goose primary hepatocyte.