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Vol. 19. Issue S1.
Abstracts of the 2020 Annual meeting of the Mexican Association of Hepatology (AMH) – XV Congreso Nacional de Hepatología (23-25 de julio)
Pages 3 (September 2020)
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Vol. 19. Issue S1.
Abstracts of the 2020 Annual meeting of the Mexican Association of Hepatology (AMH) – XV Congreso Nacional de Hepatología (23-25 de julio)
Pages 3 (September 2020)
5
Open Access
The fructose enhances the HCC progression in mice under a high intake of fructose in dieT
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L. Chávez-Rodríguez1,2, A. Simoni-Nieves1,2, A. Escobedo-Calvario1,2, M. Gerardo-Ramírez1,2, S. Salas-Silva1,2, R. Miranda-Labra1, V. Souza1, L. Bucio1, M.C. Gutiérrez-Ruiz1, L.E. Gomez-Quiroz1
1 Posgrado en Biología Experimental, Universidad Autónoma Metropolitana Iztapalapa, México
2 Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana Iztapalapa, México
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Background and aim: Hepatocellular carcinoma (HCC) is the fourth cause of cancer-related death and its incidence has been increasing in both men and women. One of the main concerns has been the consumption of hypercaloric diets mainly rich in carbohydrates such as fructose. High fructose diet is related to the development of Non-Alcoholic Fatty Liver Disease (NAFLD) and the progression of HCC since it potentiates the lipogenic pathway and the accumulation of lipids. The aim of the study is to determine the effect of a high fructose diet on the progression of HCC, induced by DEN, in C57Bl/6J mice strain.

Materials and methods: We used C57Bl/6J mice strain (both sex) with a high Fructose diet (Fru)(33% of Fructose in the drinking water, ad libitum). Fru supplementation started with 15 days old mice, two days after DEN was injected (10μg/Kg, i.p) and the treatment was ended 8 months later to evaluate the role of fructose in tumor progression by histological and biochemical tests. The protocol was approved by the UAM ethics commission.

Results: The major number of tumors were found in the Fructose+DEN (FD) mice group vs. only DEN (CWD) mice group. Triglyceride levels (TG) was evaluated in the serum with no detectable values; however, in the liver tissue the FD group showed significantly higher TG content. On the contrary, the Cholesterol (CHO) levels were significantly higher in the serum of dietary fructose group and had no differences in the tissue. The protein content in tissue followed the same observed pattern, since significance was only found in Fatty acid synthase (Fasn) with a higher protein content in the groups with dietary Fructose. Curiously, we noticed tumors in the lungs. Conclusion. The data strongly suggests that the high consumption of Fru in the diet induces effects in liver tumor promotion, in a mechanism dependent on FASN and independent of CHO. High consumption of Fru should be considered as a liver toxic factor.

This work has been partially founded by Conacyt: Fronteras de la Ciencia 1320 and by the UAM.

Conflicts of interest: The authors have no conflicts of interest to declare.

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