Neurogenic hypothesis of antiobesity action: is it on the horizon?

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Prescriptions of antiobesity medications (AOMs) have doubled since 2018, driven by GLP-1R and GIP receptor agonists like semaglutide and tirzepatide.
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AOMs reduce food intake by increasing satiety and have shown neuroprotective effects, suggesting complex mechanisms beyond their anorexigenic function.
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AOMs influence hypothalamic adult neurogenesis (hAN) by preserving hypothalamic neural stem cells and reducing cell proliferation during high-fat diet exposure.
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AOMs increase the number of newly generated neurons in the medial basal hypothalamus, potentially contributing to their weight management effects.
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Establishing a neurogenic hypothesis of obesity treatment faces challenges, as adult neurogenesis in the hypothalamus may have significant functional impacts.

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