Interval fasting and liver
Molecular "advantages" of intermittent fasting
Pathologies associated with metabolic disorders, such as diabetes mellitus or cardiovascular diseases, are becoming an increasingly heavy burden for modern society. Diets with restricted nutrition are one of the most popular and affordable ways to correct such diseases. However, not too much is known about the cellular mechanisms of their action. Recently, Australian scientists have studied , using the example of laboratory mice, how the sparing dietary scheme – intermittent fasting - affects the general condition of the body and, especially, the liver.
Recently we wrote about the results of studying the cellular mechanisms that provide the positive effects of a "hungry" diet based on constant calorie restriction. However, there are other strategies of "relative fasting": restrictions on the time of eating during the day and intermittent fasting (for example, eating every other day).
The latter is not only psychologically more comfortable compared to the usual long-term therapeutic fasting, but also has a beneficial effect on metabolism. Using laboratory animals as models, the researchers found that intermittent fasting, without causing body weight loss, improves the sensitivity of cells to insulin, reduces glucose and cholesterol levels in the blood and, as a result, increases life expectancy.
It is known that in response to prolonged fasting, a number of negative events related to the metabolism of carbohydrates and fats occur in the mammalian body. First of all, this concerns the liver. Thus, the deterioration of the insulin signaling pathway during fasting blocks the synthesis of free fatty acids and leads to the accumulation of fat in liver cells, which increases the risk of developing serious diseases such as fibrosis and cancer of this organ.
Scientists from the University of Sydney (Australia) decided to find out what happens in the body and, in particular, in the liver during intermittent fasting. To do this, they divided young male laboratory mice into two groups, one of which served as a control, and the other was fed every other day for 12 days. Since the experimental animals ate almost twice as much as usual on the feeding day, the restriction in nutrition practically did not affect their body weight. But on other indicators, the groups differed significantly.
Animals on a diet, as expected, showed better indicators of carbohydrate metabolism compared to control ones: lower baseline levels of insulin and glucose in the blood on an empty stomach, as well as the correct response to glucose loading. Analysis of the liver proteins of these mice showed that they had increased the level of enzymes involved in the synthesis of fatty acids, as well as in the cleavage of these molecules in the mitochondria – the "power stations" of the cell. One of the unexpected discoveries is the suppression of the regulatory protein HNF4a and, accordingly, its targets: bile acid synthesis enzymes, protein inhibiting enzymes that break down proteins, and proteins that cause inflammation.
Scientists conclude that such molecular effects of intermittent fasting can prevent liver obesity and activate protection against oxidative stress. All this contributes to improving glucose tolerance and, ultimately, increasing life expectancy.
The results of this experiment proved once again, but on another level, the usefulness of intermittent fasting – at least for animals. They also discovered new molecular targets (for example, the HNF4a protein) for potential drugs that could mimic the positive effects of such a diet in humans.
Article by Hatchwell et al. A Multi-omics Analysis of the Intermittent Fasting Response in Mice Identifies an Unexpected Role for HNF4a is published in the journal Cell Reports.
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