Excess Sugar Alone Induces Fatty Liver in HEPG2 Hepatocytes
Document Type
Oral Presentation
Event Website
https://source2022.sched.com/
Start Date
18-5-2022
End Date
18-5-2022
Keywords
Metabolism, Liver Disease, Biochemistry
Abstract
Liver disease affects one in every three Americans and leads to diseases such as Type II Diabetes Mellitus, hypertension, and cardiac disease. The majority of people suffering from liver disease did not abuse alcohol but rather develop fatty liver from diets high in simple sugars or sugar and fat together. These metabolically stressful diets induce steatosis and fibrosis, which is referred to as Non-Alcoholic Fatty Liver Disease (NAFLD). In this study, we used HEPG2 cells as a model for fatty liver disease caused by excess sugar, without excess fat. To look at how excess lipid accumulation impacts HEPG2 cell metabolism, we induced lipid droplet formation by feeding cells media containing different concentrations of hexoses and growth factors. rates of cells cultured in low (5mM) or high (25mM) glucose or high (25mM) fructose were measured with Crystal Violet assays. Growth rates between different groups were not significant; excess sugars did not promote faster growth, nor did it cause cell death. Oil Red O staining was used to assess intracellular lipid accumulation in excess glucose and excess fructose (with 5mM glucose), with or without growth factors. Growth factors are needed to induce lipid-laden cells; high sugar concentrations in the media alone are not sufficient. Excess lipid droplets are known to cause metabolic stress by disrupting the reduction-oxidation balance of a cell. To assess this, glutathione levels were measured. We show that excess sugars, without fat, can promote fatty liver in HEPG2 cells.
Recommended Citation
Lewis, Jennifer, "Excess Sugar Alone Induces Fatty Liver in HEPG2 Hepatocytes" (2022). Symposium Of University Research and Creative Expression (SOURCE). 66.
https://digitalcommons.cwu.edu/source/2022/COTS/66
Department/Program
Biomedical Science
Additional Mentoring Department
Biological Sciences
Additional Mentoring Department
Funding from Central OUR Grants
Excess Sugar Alone Induces Fatty Liver in HEPG2 Hepatocytes
Liver disease affects one in every three Americans and leads to diseases such as Type II Diabetes Mellitus, hypertension, and cardiac disease. The majority of people suffering from liver disease did not abuse alcohol but rather develop fatty liver from diets high in simple sugars or sugar and fat together. These metabolically stressful diets induce steatosis and fibrosis, which is referred to as Non-Alcoholic Fatty Liver Disease (NAFLD). In this study, we used HEPG2 cells as a model for fatty liver disease caused by excess sugar, without excess fat. To look at how excess lipid accumulation impacts HEPG2 cell metabolism, we induced lipid droplet formation by feeding cells media containing different concentrations of hexoses and growth factors. rates of cells cultured in low (5mM) or high (25mM) glucose or high (25mM) fructose were measured with Crystal Violet assays. Growth rates between different groups were not significant; excess sugars did not promote faster growth, nor did it cause cell death. Oil Red O staining was used to assess intracellular lipid accumulation in excess glucose and excess fructose (with 5mM glucose), with or without growth factors. Growth factors are needed to induce lipid-laden cells; high sugar concentrations in the media alone are not sufficient. Excess lipid droplets are known to cause metabolic stress by disrupting the reduction-oxidation balance of a cell. To assess this, glutathione levels were measured. We show that excess sugars, without fat, can promote fatty liver in HEPG2 cells.
https://digitalcommons.cwu.edu/source/2022/COTS/66
Faculty Mentor(s)
Sarah Oppelt