PEI-NI CHENSHUN-FA YANGCHING-HAN YU2026-10-162026-10-162011-10-15Pure ID: 15066043Pure UUID: 9dfbd578-1aa7-48a0-92a8-feafe553a56610.1089/ars.2010.3738https://www.scopus.com/pages/publications/80052589527https://scholars.csmu.edu.tw/handle/123456789/29972Aims: Studies have reported that redox signaling in the hypothalamus participates in nutrient sensing. The current study aimed to determine if the activation of reactive oxygen species-related enzymes (ROS-RE) in the hypothalamus participates in regulating neuropeptide Y (NPY)-mediated eating. Moreover, possible roles of proopiomelanocortin (POMC) and atypical protein kinase C (aPKC) were also investigated. Rats were treated daily with phenylpropanolamine (PPA) for 4 days. Changes in the expression levels of ROS-RE, POMC, NPY, and aPKC were assessed and compared. Results: Results showed that ROS-RE, POMC, and aPKC increased, with a maximal response on Day 2 (anorectic effect) and with a restoration to the normal level on Day 4 (tolerant effect). By contrast, NPY expression decreased, and the expression pattern of NPY proved opposite those of ROS-RE and POMC. Central inhibition of ROS production by ICV infusion of ROS scavenger attenuated PPA anorexia, revealing a crucial role of ROS in regulating eating. Cerebral aPKC knockdown by ICV infusion of antisense aPKC modulated the expression of ROS-RE, POMC, and NPY. Conclusion: Results suggest that ROS-RE/POMC-and NPY-containing neurons function reciprocally in regulating both the anorectic and tolerant effects of PPA, while aPKC is upstream of these regulators. Innovation: These results may further the understanding of ROS-RE and aPKC in the control of PPA anorexia.13enjournal article