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ePoster
RAB23 CONTROLS APPETITE VIA CILIARY REGULATION OF THE LEPTIN-MELANOCORTIN PATHWAY IN HYPOTHALAMUS NEURONS
Catherine Hong Huan Hor
Hong Kong Baptist University
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-593
Presentation
Date TBA
Board: PS03-08AM-593
Event Information
Poster Board
PS03-08AM-593
Poster
View posterAbstract
Rab23 is known to mediate primary cilium formation, ciliary trafficking and the Hedgehog signaling pathway. In humans, biallelic mutations of RAB23 cause Carpenter syndrome, which is commonly associated with childhood obesity. The underlying mechanisms by which the loss of Rab23 leads to obesity remain largely elusive. Here, we demonstrate that conditional knockout (CKO) of Rab23 in the mouse brain, and adeno-associated virus (AAV)-driven deletion of Rab23 in the adult hypothalamus neurons, both result in increased body weight and food intake, as well as a compromised response to leptin and Mc4r agonist, Setmelanotide. Intriguingly, we observed profound deciliation and concomitant dysregulation of leptin-melanocortin signaling response in Rab23-KO hypothalamus neurons, indicating that impaired ciliary function may contribute to leptin resistance and hyperphagic obesity in Rab23 mutant mice. Collectively, our findings reveal a novel role for Rab23 in the hypothalamic regulation of satiety via the ciliary leptin-melanocortin signaling pathway.
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