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.  Continue reading

One Fatty Meal Results In Metabolic Disturbances

MedicalResearch.com Interview with:

Prof. Dr. Michael Roden Director, German Diabetes Center (DDZ) Leibniz Center for Diabetes Research at Heinrich Heine University Düsseldorf Chair/Professor, Endocrinology and Metabolic Diseases Heinrich Heine University Düsseldorf Director, Department of Endocrinology and Diabetology University Hospital Düsseldorf Düsseldorf, Germany

Prof. Michael Roden

Prof. Dr. Michael Roden
Director, German Diabetes Center (DDZ)
Leibniz Center for Diabetes Research
at Heinrich Heine University Düsseldorf
Chair/Professor, Endocrinology and Metabolic Diseases
Heinrich Heine University Düsseldorf
Director, Department of Endocrinology and Diabetology
University Hospital Düsseldorf
Düsseldorf, Germany

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: The prevalence of obesity, type 2 diabetes and non-alcoholic fatty liver disease (NAFLD) continue to increase at an alarming rate. Their occurrence has been associated with intake of saturated fats, for example that of palm oil. This study aimed to shed light on how dietary fat initiates metabolic changes which lead to the aforementioned diseases. To this end we provided 14 young healthy volunteers an oral dose of palm oil or placebo randomly, in a crossover manner, with an 8-week washout period between each intervention.

One acute dose of palm oil leads to insulin resistance in the main insulin sensitive tissues of the body: the liver, skeletal muscle and adipose tissue. In the liver, it also results in increased accumulation of triglycerides, increased production of glucose from lipid and amino acid precursors (rather than from glycogen), and increased energy metabolism, as denoted by increased hepatic adenosine triphosphate (ATP) content. Moreover, a similar experiment in mice revealed that one dose of palm oil differentially regulates genes and pathways which are known or suspected regulators of NAFLD, such as lipopolysaccharide (LPS), members of the peroxisome proliferator-activated receptor (PPAR) family and nuclear factor kappa-light-chain-enhancer of activated B-cells.

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Fatty Liver At Least Partially Mediated By Epigenetic Influences

MedicalResearch.com Interview with:

Annette Schürmann PhD Department of Experimental Diabetology German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE) Nuthetal Germany German Center for Diabetes Research (DZD München-Neuherberg Germany

Dr. Annette Schürmann

Annette Schürmann PhD
Department of Experimental Diabetology
German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE)
Nuthetal
Germany German Center for Diabetes Research (DZD
München-Neuherberg Germany

MedicalResearch.com: What is the background for this study?

Response: The aim of our study was to clarify why genetically identical mice respond very different to a high fat diet. Some of the mice react with an elevated body weight, others not. We analyzed the expression pattern
of liver at two time points, at the age of 6 weeks, (the earlierst time
point to distiguish between those that respond to the diet (responder
mice) and those that did not (non-responders)), and at the age of 20
weeks. One transcript that was significantly reduced in the liver of
responder mice at both time points was Igfbp2. The reason for the
reduced expression was an elevated DNA-methylation at a position that is
conserved in the mouse and human sequence. The elevated DNA-methylation
of this specifc site in human was recently described to associate with
elevated fat storage (hepatosteatosis) and NASH. However, as 6 weeks old
mice did not show differences in liver fat content between responder and
non-responder mice we conclude that the alteration of Igfbp2 expression
and DNA metyhlation occurs before the development of fatty liver.

Our data furthermore showed that the epigenetic inhibition of Igfbp2
expression was associated with elevated blood glucose and insulin
resistance but not with fatty liver.

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