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In a study published in Science on April 15, researchers at the Weizmann Institute of Science, together with colleagues from the Queen Mary University of London and the Hebrew University of Jerusalem, have revealed the mechanism of action of the master switch for hunger in the brain: the melanocortin receptor 4, or MC4 receptor for short.
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They have also clarified how this switch is activated by setmelanotide Imcivreea drug recently approved for the treatment of severe obesity caused by certain genetic changes. These findings shed new light on the way hunger is regulated and may help develop improved anti-obesity medications. Link MC4 receptor is present in a brain region ppurpose the hypothalamus—within a cluster of neurons that compute the body's energy balance by processing a variety of energy-related metabolic signals. When the MC4 is activated, or "on"—as it normally is—it sends out commands that cause us to feel full, which means that from the brain's perspective, purpose of the hunger games default state is satiety. When our energy levels drop, the hypothalamic cluster produces a "time to eat" hormone that inactivates, or turns off the MC4 receptor, sending out a "become hungry" signal.
After we eat, a second, "I'm full" hormone is released. It binds to the same active site on the MC4, replacing the hunger hormone and turning the receptor back on—bringing us back to the satiety default.
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Mutations that inactivate purpose of the hunger games MC4 cause people to feel constantly hungry. MC4 is a prime target for anti-obesity drugs, such as setmelanotide, precisely because it's a master switch: turning it on can control hunger while bypassing all other energy-related signals. But until now it was unknown how exactly this hunger switch works. The new study began with the predicament of one family, in which at least eight members, plagued by persistent hunger, were severely obese—most of them with a body mass index of over 70, that is, about triple the norm.
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Their medical history came to the attention of Hadar Israeli, a pupose student pursuing Ph. Israeli was struck by the fact that the family's plight was due to a single mutation that ran in the family: one affecting the MC4 receptor. She turned to Dr. Moran Shalev-Benami of Weizmann's Chemical and Structural Biology Department, asking whether new advances in electron microscopy could help explain how this particular mutation could produce such a devastating effect.
Shalev-Benami launched a study purpose of the hunger games the structure of MC4, inviting Israeli to join her lab as a visiting scientist. Together with Dr. Oksana Degtjarik, a postdoctoral fellow in the lab, Israeli isolated large quantities of pure MC4 receptor from cell membranes, let it bind with setmelanotide and determined its 3D structure using cryogenic electron microscopy. The study was conducted in collaboration with the teams of Dr. Peter J. https://digitales.com.au/blog/wp-content/custom/general-motors-and-the-affecting-factors-of/erik-eriksons-theory.php Y. Niv from the Hebrew University of Jerusalem.
The 3D structure revealed that setmelanotide activates the MC4 receptor by entering its binding pocket—that is, by directly hitting the molecular switch that signals satiety, even more potently than the natural satiety hormone. It also turned out that the drug puprose a surprising helper: an ion of calcium that enters the pocket, purpose of the hunger games the drug's binding to the receptor. In biochemical and computational experiments, the scientists found that similarly to the drug, calcium also assists the natural satiety hormone.
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McCormick: "Calcium helped the satiety hormone activate the MC4 receptor while interfering with the hunger hormone and reducing its activity. The study has explained how mutations in the MC4 receptor can interfere with this signaling, leading to never-ending hunger and ultimately obesity. Moreover, the scientists have identified huner that crucially distinguish MC4 from similar receptors in the same family.
This should make it possible to design drugs that will bind only to MC4, avoiding side effects that may be caused by interactions with other receptors. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without pudpose written permission.
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