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Researchers identify epigenetic changes that increase risk of type 2 diabetes



Small chemical changes in the building blocks of DNA, which may be influenced by lifestyle factors, may reduce the amount of IGFBP2. A DIFE / DZD research group has now reported in the journal Diabetes that these epigenetic changes increase the risk of type 2 diabetes. In addition, people with high blood levels of the IGFBP2 binding protein are less likely to develop this metabolic disorder. Changes in blood are already detectable a few years before the onset of the disease.

According to the German Health Report 2018, more than 5.7 million people in Germany suffer from type 2 diabetes. Those affected react inadequately to hormonal insulin, which leads to high levels of blood glucose . This in turn can lead to strokes, heart attacks, damage to the retina, damage to the kidneys and nervous disorders. Because the metabolic disease develops gradually, the initial damage has already occurred at the time of diagnosis. "In the future, our findings could help identify potential risk factors for type 2 diabetes even earlier and help counter the disease with preventive measures," said Professor Annette Schürmann, head of the Department of Experimental Diabetology at the # 39, German Institute of Human Nutrition Potsdam-Rehbruecke (DIFE) and speaker of the German Center for Diabetes Research (DZD).

Discovering Molecular Mechanisms

In addition to insulin, insulin-like growth factor 1

(IGF-1) is also involved in the metabolism of sugar and fat. The effect of this growth factor is weakened by binding to the IGF-binding protein 2 (IGFBP2). If the liver does not release enough IGFBP2 into the blood, the balance of glucose and lipid metabolism can be discontinued. The research team led by Schürmann and Professor Matthias Schulze, head of the Department of Molecular Epidemiology at DIfE, then investigated how the reduced effect of the IGFBP2 gene could influence the development of type 2 diabetes.

# 39; man show that people suffering from the fatty liver produces and releases less IGFBP2. The Schürmann team observed similar effects in previous experiments with mice, which showed that IGFBP2 levels were already reduced before hepatic disease. This is due to the transfer of methyl groups to some sites of the DNA sequence IGFBP2, which inhibited the gene in the liver. These so-called epigenetic changes are caused, among other things, by factors related to lifestyle. Such DNA modifications in the IGFBP2 gene were also previously detected in the blood cells of overweight people with impaired glucose tolerance.

Translational research from mice to human studies

The interdisciplinary research group led by Schürmann and Schulze used the results of the clinic and laboratory to evaluate blood samples and data from EPIC Potsdam. "This study is a good example of how translational research works: a clinical finding is collected, mechanically analyzed in the laboratory and finally examined in a population study," said Schürmann.

Recent analysis by researchers indicates that inhibition of the IGFBP2 gene promotes type 2 diabetes. In addition, the team of scientists noted that the slimmest study participants and study participants with lower hepatic fat levels they had higher concentrations of the protective binding protein in the blood. Plasma concentrations higher than IGFBP2 were associated with a lower risk of developing type 2 diabetes in later years. "Our study confirms the hypothesis that the IGF-1 signaling pathway also plays an important role in the development of type 2 diabetes in humans," added Dr. Clemens Wittenbecher, associate researcher at the Department of Molecular Epidemiology at DIFE and first author of the. study

Source:

http://dzd-ev.de/en/latest/news/news/article/new-marker-provides-insights-into-the-development-of-type-2- diabetes / index.html


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