Alcohol, Author Interviews, Hepatitis - Liver Disease, Lifestyle & Health, Sugar / 25.04.2019
Replacing Alcohol with Soda Not Good for the Liver
MedicalResearch.com Interview with:
E. van Eekelen, MSc | PhD Candidate
Leiden University Medical Center
Dept. Clinical Epidemiology
Leiden, The Netherlands
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Fatty liver, defined as excess accumulation of fat within the liver, covers a broad clinical spectrum and is the leading cause of chronic liver diseases. It has also been linked to type 2 diabetes and cardiovascular disease.
The consumption of alcohol is a well-established risk factor for fatty liver. However, we hypothesized that consumption of non-alcoholic energy-containing beverages also leads to liver fat accumulation. We analysed data from the Netherlands Epidemiology of Obesity (NEO) study, which is a prospective population-based cohort study including non-invasive measurements of liver fat content by magnetic resonance spectroscopy. Besides consumption of alcoholic beverages, sugar sweetened beverages were associated with more liver fat. We specifically showed that replacement of alcoholic beverages with milk was associated with less liver fat, whereas replacement with sugar sweetened beverages was associated with a similar amount of liver fat, even when taking calories into account.

Dr. Nahmias[/caption]
MedicalResearch.com Interview with:
Prof. Yaakov Nahmias PhD
Director of the Alexander Grass Center for Bioengineering
Hebrew University of Jerusalem
Medical Research: What is the background for this study?
Prof. Nahmias: The liver has a limitless capacity of the human liver to regenerate from even a massive loss of mass.
However, the intrinsic capacity of liver cells to proliferate is lost when cells are removed from the body.
Medical Research: What are the main findings?
Prof. Nahmias: We found that a weak expression of Human Papilloma Virus (HPV) proteins released hepatocytes from cell-cycle arrest and permitted the cells to multiply in response to Oncostatin M (OSM) an immune cytokine recently found to be involved in liver regeneration.
While previous efforts caused hepatocytes to multiply without control, converting hepatocytes into tumor cells with little metabolic ability, we selected colonies that only multiply in response to OSM.
Activation with OSM triggered cell growth with a doubling time of 40 hours. Removal of OSM caused growth to stop, allowing the cells to regain a high level of metabolic activity within 4 days.
We produced hepatocytes from ethnically diverse individuals. Importantly, the growing hepatocytes showed a similar toxicology response to normal human hepatocytes across 23 different drugs.
