PEI-NI CHENCHING-HAN YU2026-10-162026-10-162014-07-01Pure ID: 14967293Pure UUID: e7d3ba0e-8ae4-4f90-9a89-b910f313267910.1111/bph.12667https://www.scopus.com/pages/publications/84902212522https://scholars.csmu.edu.tw/handle/123456789/27227Background and Purpose Appetite suppression induced by amphetamine has been attributed to its inhibition of neuropeptide Y (NPY) neurons and activation of pro-opiomelanocortin (POMC) neurons in the hypothalamus. This study examined whether STAT3 was involved in these actions of amphetamine. Experimental Approach Rats were given amphetamine daily for 4 days. Changes in the expression of NPY, POMC, melanocortin MC3 receptors, PI3K and STAT3 in the hypothalamus were assessed by RT-PCR and Western blotting. Antisense oligonucleotides to STAT3 were also used. Key Results Expression of NPY decreased with a maximum effect day 2 of amphetamine treatment. Expression of POMC, MC3 receptors, PI3K and STAT3 increased with a maximum response on day 2. Moreover, phosphorylation of STAT3 and its DNA binding activity increased and was expressed in a similar pattern. Infusion (i.c.v.) of STAT3 antisense at 60-min before amphetamine treatment, partly blocked amphetamine-induced anorexia and modulated expression of NPY, POMC, MC 3 receptors and PI3K, indicating the involvement of STAT3 in amphetamine-treated rats. Conclusions and Implications Hypothalamic PI3K-STAT3 signalling participated in the regulation of NPY- and POMC-mediated appetite suppression. These findings may contribute to a better understanding of anorectic drugs.11enjournal article