Title

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.

Faculty Mentor(s)

Sarah Oppelt

Department/Program

Biomedical Science

Additional Mentoring Department

Biological Sciences

Additional Mentoring Department

Funding from Central OUR Grants

Streaming Media

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May 18th, 12:00 AM May 18th, 12:00 AM

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