Introduction

In the past and in the present day, fasting is a common practice throughout the world. For example, many patients are asked to fast before operations or certain medical examinations. Sometimes fasting is also used to make a political statement, usually a protest. Many athletes and people who want to lose weight and maintain muscle mass practice intermittent fasting. Another very popular reason is religious views, such as: B. the month of Ramadan.

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

How does fasting affect our epigenetics?

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

Current research

Compared to normally fed mice, an increase in the expression levels of HDAC3 and -4 and a decrease in the expression levels of HDAC10 and -11 were found in the medial hypothalamus of fasted mice [2]. Furthermore, in the same study, lower numbers of cells with acetylated histones H3 and H4 were observed in the ventromedial hypothalamic nucleus (VMH), which play a crucial role in aggression and reproductive behavior [2,3,4]. The direct impact of these histone modifications is not yet clear; however, it suggests that during fasting, the role of HDAC3 and -4 promotes deacetylation in the VMH, leading to altered gene expression and function.

In another study, mice were subjected to four cycles of 72 hours (3 days) of intermittent fasting followed by 96 hours (4 days) of normal feeding [5]. Higher levels of histone acetylation were observed in the promoter region of mitochondria-activating genes (ACO and UCP1). These changes suggest increased expression of these genes as physical endurance was improved following the intermittent fasting cycles [5].

Conclusion

Ultimately, fasting, like other environmental factors, appears to have an impact on our epigenetic profiles. Although very little is known about how fasting directly affects our epigenetics, there is much ongoing research into the connections between epigenetic changes and fasting. This is a good example that there is still a lot to be researched in the field of epigenetics. Uncovering, detecting and quantifying such mechanisms and changes that influence our epigenome is what we do at MoleQlar Analytics.