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    They identify the origin of the vicious circle that makes you gain weight in the brain | Health & Wellness

    The abundance of tasty foods high in fat or sugar has led to more long-lived people, but has also led to an epidemic of obesity-related diseases that leads to poor health and tests the resilience of healthcare systems. One of the ways to put a stop to this health crisis is in the study of what happens in the brain when we are exposed to certain foods. This week, a team led by Michiru Hirasawa, from the Memorial University of Newfoundland (Canada), publishes a paper in the journal PNAS in which they try to understand the relationship between inflammation of the hypothalamus, a part of the brain that regulates energy balance and our sense of hunger, and the consumption of high-fat diets.

    It has long been known that high-fat diets can lead to a vicious cycle that is difficult to stop. These foods produce inflammation of the hypothalamus that increases appetite to levels that make us eat more than we need and gain weight. However, scientists have also observed an apparently paradoxical effect. Inflammation in that region of the brain is also associated with diseases such as anorexia and others that cause weight loss. Hirasawa and his collaborators used animal models to try to find the way in which this relationship between inflammation and disordered appetite is regulated.

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    In their work, the researchers show that high-fat diets cause prostaglandin E2 (PGE2), a molecule that regulates immune system processes such as fever, to activate the MHC hormone in the hypothalamus, which makes us feel hungry. This mechanism may also explain why brain inflammation sometimes leads to weight gain and excessive loss at other times. If it is found in a high concentration and produces intense inflammation, PGE2 suppresses the appetite, but if the concentration is lower, it increases it.

    The authors of the work verified that, by genetically modifying the mice with which the study was carried out, the receptors for this prostaglandin in the MHC neurons were eliminated, the animals were protected against obesity or fatty liver that caused inflammation of the hypothalamus linked to by a high-fat diet.

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    Hirasawa acknowledges that it is not easy to predict “the result of inflammation, because low or high intensity is relative, it can be acute or chronic and involve many different organs, cells and molecules.” However, although they produce different ailments, “reducing inflammation can alleviate both symptoms.” For this reason, the researcher proposes that any strategy that achieves this effect can be useful from many points of view. “For example, the Mediterranean diet is anti-inflammatory and is known to help reduce weight in people who are overweight or obese.” Lastly, she cautions that it is also essential to be selective about how and when anti-inflammatory treatments are used, as inflammation is also necessary for our daily functioning, for example healing wounds or fighting infections.

    At a time when some forecasts suggest that within less than a decade up to 80% of men and 55% of women will be overweight or obese, and when weight-loss drugs are becoming blockbusters, the possibility of finding therapeutic targets against uncontrolled appetite arouses great interest. Hirasawa believes that his findings “may one day lead us to treatments for obesity.” Knowledge of the mechanism that starts with the intake of fatty foods and causes inflammation that increases appetite would allow the development of treatments that use this target. The genetic modification to which the mice were subjected in the study published in PNAS It seems like a very radical option and we must bear in mind that PGE2 has many other functions, apart from inflaming the hypothalamus and making us hungry. “It is to be expected that treatments that block this mechanism will have an anti-obesity effect,” says Hirasawa. However, she concludes, “it is critical to identify possible side effects and test their safety before using them.”

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    Source: EL PAIS

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