Eine neue Studie an Mäusen legt nahe, dass das Gehirn eine Schlüsselrolle bei der Kontrolle des Körpergewichts spielt, indem es die Fettaufnahme im Darm reguliert | Ein Gehirn-Darm-Signal steuert die Fettaufnahme im Darm

From the news report:

>But, contrary to the somewhat intuitive idea that this absorption takes place autonomously by passive diffusion in the digestive system, we now know that it is also controlled by the brain, and a large and coordinated group of researchers from hospitals and universities in Shanghai, China, has just revealed the precise mechanism by which this control takes place in mice. The characteristics of their research, published in the prestigious journal Nature, are explained below, adding context to apply it to humans.
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>The first signs indicating the presence of nutrients in the digestive tract reach the brain via the vagus nerve, the tenth of the cranial nerve pairs in humans and the longest and most important nerve in the autonomic nervous system for digestion and energy homeostasis. The bodies of its neurons are found in four nuclei of the brain stem, specifically in the medulla oblongata, and its terminals extend throughout the digestive tract, innervating organs such as the stomach, the portal vein and the crypts and valleys of the entire intestine. Its winding and vague course through the interior of the body is what gives it its name. Much of the function of the vagus nerve is parasympathetic, which is why it is part of the autonomic nervous system responsible for anabolism, that is, limiting expenditure and promoting energy increase and saving.
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>Now, the aforementioned Chinese researchers have shown that, in addition to the vagus nerve’s known regulation of gastric motility and digestive processes, chemically inactivating its dorsal motor nucleus in mice reduces intestinal fat absorption, causing them to lose body weight. Likewise, activating this same nucleus causes the opposite effect, increasing intestinal fat absorption and body weight.
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>But the most novel and surprising thing that researchers have observed is that when a certain group of neurons in that same nucleus is deactivated, specifically those that project to the jejunum, a part of the small intestine, the length of the microvilli in the intestinal wall is shortened, which reduces its surface area and thus the place in whose blood capillaries fat absorption occurs. The brain thus regulates this absorption by controlling the length and surface area of the intestinal spaces in which it takes place.

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Link to the journal: [A brain-to-gut signal controls intestinal fat absorption](https://www.nature.com/articles/s41586-024-07929-5)

Abstract:

>Although fat is a crucial source of energy in diets, excessive intake leads to obesity. Fat absorption in the gut is prevailingly thought to occur organ-autonomously by diffusion. Whether the process is controlled by the brain-to-gut axis, however, remains largely unknown. Here we demonstrate that the dorsal motor nucleus of vagus (DMV) plays a key part in this process. Inactivation of DMV neurons reduces intestinal fat absorption and consequently causes weight loss, whereas activation of the DMV increases fat absorption and weight gain. Notably, the inactivation of a subpopulation of DMV neurons that project to the jejunum shortens the length of microvilli, thereby reducing fat absorption. Moreover, we identify a natural compound, puerarin, that mimics the suppression of the DMV–vagus pathway, which in turn leads to reduced fat absorption. Photoaffinity chemical methods and cryogenic electron microscopy of the structure of a GABAA receptor–puerarin complex reveal that puerarin binds to an allosteric modulatory site. Notably, conditional Gabra1 knockout in the DMV largely abolishes puerarin-induced intestinal fat loss. In summary, we discover that suppression of the DMV–vagus–jejunum axis controls intestinal fat absorption by shortening the length of microvilli and illustrate the therapeutic potential of puerarin binding to GABRA1 in fat loss.

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nb: reposted from earlier with modified headline