AIM: In the present study, we examined the expression and function of miR-15b in a rat model of non-alcoholic fatty liver disease (NAFLD), and we determined whether the presence of miR-15b in serum can be used as a biomarker for this disease. METHODS: We measured the expression of miR-15b in both the high-fat-induced non-alcoholic fatty liver disease (NAFLD) SD rat model and in the palmitate-induced NAFLD L02 cell model. Following transfection of miR-15b into QSG7701 cells, cell proliferation, glucose consumption and intracellular triglyceride levels were measured. We also measured the levels of miR-15b in the serum of fatty liver disease patients using real-time PCR. RESULTS: We found that miR-15b was upregulated in the livers of NAFLD SD rats as well as in NAFLD L02 cells. Increased miR-15b levels could cause decreased cell proliferation and glucose consumption as well as induce the storage of intracellular triglyceride in QSG7701 cells. The expression of miR-15b was also significantly elevated in the serum of fatty liver disease patients compared with healthy subjects. CONCLUSIONS: Increased miR-15b expression in NAFLD models may lead to decreased cell proliferation and glucose consumption while inducing the storage of intracellular triglyceride, which are all hazards of NAFLD. Therefore, increased serum miR-15b level is a potentially biomarker for the diagnosis of fatty liver disease.
AIM: In the present study, we examined the expression and function of miR-15b in a rat model of non-alcoholic fatty liver disease (NAFLD), and we determined whether the presence of miR-15b in serum can be used as a biomarker for this disease. METHODS: We measured the expression of miR-15b in both the high-fat-induced non-alcoholic fatty liver disease (NAFLD) SD rat model and in the palmitate-induced NAFLD L02 cell model. Following transfection of miR-15b into QSG7701 cells, cell proliferation, glucose consumption and intracellular triglyceride levels were measured. We also measured the levels of miR-15b in the serum of fatty liver diseasepatients using real-time PCR. RESULTS: We found that miR-15b was upregulated in the livers of NAFLD SD rats as well as in NAFLD L02 cells. Increased miR-15b levels could cause decreased cell proliferation and glucose consumption as well as induce the storage of intracellular triglyceride in QSG7701 cells. The expression of miR-15b was also significantly elevated in the serum of fatty liver diseasepatients compared with healthy subjects. CONCLUSIONS: Increased miR-15b expression in NAFLD models may lead to decreased cell proliferation and glucose consumption while inducing the storage of intracellular triglyceride, which are all hazards of NAFLD. Therefore, increased serum miR-15b level is a potentially biomarker for the diagnosis of fatty liver disease.
Authors: Fatjon Leti; Ivana Malenica; Meera Doshi; Amanda Courtright; Kendall Van Keuren-Jensen; Christophe Legendre; Christopher D Still; Glenn S Gerhard; Johanna K DiStefano Journal: Transl Res Date: 2015-05-04 Impact factor: 7.012