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Significance The dorsomedial hypothalamus (DMH) is well known for its role in the regulation of energy expenditure; however, its role in the control of appetite is less defined. Our study identifies TrkB-expressing DMH neurons that potently suppress appetite and efficiently maintain physiological satiety when they are activated. Furthermore, because ablating the TrkB receptor in these neurons increased appetite and reduced energy expenditure, our study indicates that BDNF could act in part on the DMH to control body weight. These results suggest that activation of DMH TrkB neurons could be a powerful way to treat obesity because it will not only greatly reduce appetite but also overcome a potent counterregulatory mechanism by which food restriction-induced weight loss disproportionately reduces energy expenditure.

TrkB-expressing neurons in the dorsomedial hypothalamus are necessary and sufficient to suppress homeostatic feeding