Introduction

In the past and today, fasting all over the world is a common practice. For example, many patients are asked to fast, before operations or certain medical examinations. Sometimes fasting also serves to set a political sign, usually a protest. Many athletes and people who want to lose weight and want to preserve their muscle mass practice intermittent fasting. Another very popular reason are religious views, such as: B. the month Ramadan.

Well -controlled, reasonable fasting patterns, according to which the individual continues to maintain a healthy lifestyle, are associated with several health advantages. These advantages include improving blood sugar control, weight loss and initiating the cell repair [1]. But what is the reason for these clear differences? And does it happen to do something with our epigenetical profile?

How does fasting affect our epigenetics?

Just as many environmental factors cause epigenetic changes, fasting has been shown to have an impact. In response to fasting, for example, there are changes in the expression of neuropeptides in the medial hypothalamus that regulate the feeding and metabolic behavior [2]. In mice, it was shown that the expression of histone deacetylases (HDACS) is influenced in the medial hypothalamus by fasting. In the broadest sense, HDACs are enzymes that are responsible for the removal of acetyl groups from histones and are known for their participation in the epigenetic control of gene expression.

Current research

Compared to normally fed mice, an increase in the expression values ​​of HDAC3 and -4 and a decline in the expression values ​​of HDAC10 and -11 was found in the medial hypothalamus of frowned mice [2]. In addition, a smaller number of cells with acetylated histones H3 and H4 in the ventromedial hypothalamic core (VMH) were observed in the same study, which play a crucial role in aggression and reproduction behavior [2,3,4]. The direct impact of these histone modifications has not yet been clarified; However, it indicates that during fasting the role of HDAC3 and -4 promotes the deacetylation in the VMH, which leads to a changed gene expression and function.

In another study, mice were subjected to four cycles of 72 hours (3 days) intermittent fasting, followed by 96 hours (4 days) normal feeding [5]. In the promoter region of mitochondria -activating genes (ACO and UCP1), higher histoneacetylation were observed. These changes indicate increased expression of these genes, since physical endurance after the intermittent fasting cycles has been improved [5].

conclusion

Ultimately, fasting, like other environmental factors, seems to have an impact on our epigenetic profiles. Although very little is known about how fasting has a direct impact on our epigenetics, there are many ongoing research on the connections between epigenetic changes and fasting. This is a good example of the fact that there is still a lot to explore in the field of epigenetics. The detection, detection and quantification of such mechanisms and changes that influence our epigenoma is what we do in moleqlar analytics.