At the molecular level
Starvation triggered autophagy and forced cells to process protein "garbage" more actively
Maria Azarova, Naked Science
The modern lifestyle and the popularity of fast food, emotional relief through eating delicious and high–calorie food, and much more have led to the fact that in the last decades the problem of obesity has been hanging over the world – in particular, developed countries. For example, in the UK, which among the countries of Western Europe was particularly prone to obesity, overweight among its population began to occur three times more often in 30 years. According to experts, by 2050, more than half of the inhabitants of the United Kingdom will suffer from weight problems. There is no need to remind you once again that obesity increases the risk of developing many diseases and, eventually, death.
Many research teams are engaged in the search for truly effective methods for losing weight (and it's not so much about the aesthetic side of the issue as about human health). Including scientists from the University of Warwick (Coventry, UK), who in their study published in the journal Cell Reports (Jacomin et al., Self-Regulation of Autophagy Genes Expression by Atg8a and Its Interacting Partners YL-1, Sequoia and Sir2 In Drosophila), studied how cells respond to therapeutic fasting is a voluntary refusal of food (and sometimes water) followed by the correct "exit" – and activates a process called autophagy.
Intermittent fasting (alternating the period of hunger with "windows" when you take food for one day), fasting after a day and other forms of periodic restriction of food intake are useful for maintaining a healthy weight and have gained particular popularity in recent years. As a response to starvation, cells use autophagy – the process of cellular self-healing; this is the natural mechanism of the cell, which disassembles unnecessary or dysfunctional components, processes the so-called cellular debris, gets rid of damaged organelles, and so on.
A group of scientists led by Professor Ioannis Nezis found out how cells activate autophagy genes during fasting. As part of the study, the authors of the work raised several groups of fruit fly larvae: the first group ate in accordance with the usual regime, and the second practiced fasting.
After that, cells were taken from several experimental subjects to study the activity of genes and proteins associated with autophagy. As a result, scientists have discovered three types of protein molecules necessary for transcription of autophagy genes and the active launch of this process in starving flies. Thus, Sequoia, YL-1 and Sir2 proteins interact with the cytoplasmic protein associated with autophagy – Atg8a, then they "recruit" Atg8a in the nucleus to control transcription of autophagy genes.
At the same time, Sequoia blocked its activation, and YL-1 and Sir2 were responsible, on the contrary, for triggering this mechanism. To confirm the role of these proteins, the authors of the study blocked the genes associated with the production of YL-1 and Sir2: after that, autophagy in fruit flies was not activated even with prolonged fasting.
"Understanding the molecular mechanisms of autophagy gene activation during fasting will help us use interventions to activate autophagic pathways to maintain a normal body weight and promote a healthy lifestyle," says Nezis.
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