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Our previous result showed in the fatty liver formation induced-by overfeeding goose, it was accompanied by an activation of PI3K-Akt-mTOR pathway and an increase of plasma insulin concentration. Recent studies have suggested a crucial role for PI3K-Akt-mTOR pathway in regulating cell proliferation, so we hypothesize that insulin acts goose hepatocellular growth by PI3K-Akt-mTOR signal pathway. Here we first showed that insulin evidently increased the cell DNA synthesis rate, rate of BrdU-positive cells, the mRNA level and protein content of factors involved in the cell proliferation of goose primary hepatocytes. Meanwhile, insulin evidently increased the mRNA level and protein content of factors involved in PI3K-Akt-mTOR pathway. However, the up-regulation of insulin on cell proliferation was decreased significantly by the inhibitors of PI3K-Akt-mTOR pathway, LY294002, rapamycin or NVP-BEZ235. These findings suggest that PI3K-Akt-mTOR pathway plays an essential role in insulin-regulated cell proliferation of goose hepatocyte. |
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Keywords:insulin; PI3K-Akt-mTOR signal pathway; cell proliferation |
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