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    Home > Biochemistry News > Biotechnology News > Researchers identify brain region linked to satiety

    Researchers identify brain region linked to satiety

    • Last Update: 2022-03-08
    • Source: Internet
    • Author: User
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    Feeling full after a meal is healthy and normal, but the reasons for this feeling are complex and not well understood


    Currently, there are six drugs approved by the Food and Drug Administration (FDA) for weight control, but they often have side effects


    "When we can more precisely target the part of the brain responsible for satiety, we can create treatments with fewer side effects," said the study's lead author Haijiang Cai, an associate professor in the School of Neuroscience


    Previous research has mapped the satiety circuit to the brain's amygdala center, which also controls fear, pain and other strong emotions


    Cai and his team found that after the amygdala, signals are sent to a neuron located in the brain called the parahypothalamic nucleus (PSTh), which is responsible for satiety


    Here's how they do it: First, they know that the gut-secreted hormone cholecystokinin (CCK) tells the brain "I'm full" after a meal


    In a mouse model, the researchers determined that neurons activated by CCK and PKC-delta neurons were located in the parathalamic nucleus


    The brain's PSTh region was first discovered by Chinese scientists in the 1990s and introduced into English-language scientific literature in 2004, but its function is unknown


    "We found that neurons in this region are required for CCK saturation to inhibit feeding," Cai said


    Feeling content is so important that Cai suspects it is mediated by one area of ​​the brain; more likely, multiple areas of the brain work together


    Cai started studying the neural circuits of eating because he was intrigued by the role emotions play in our eating habits


    "We know eating and mood are different behaviors, but they interact closely with each other," he said


    article title

    Dissecting a disynaptic central amygdala-parasubthalamic nucleus neural circuit that mediates cholecystokinin-induced eating suppression

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