Antioxidants & redox signaling · 2011
Role of reactive oxygen species-related enzymes in neuropeptide y and proopiomelanocortin-mediated appetite control: a study using atypical protein kinase C knockdown.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Kuo Dong-Yih, Chen Pei-Ni, Yang Shun-Fa, Chu Shu-Chen, Chen Chin-Hsiu, Kuo Meng-Hsien, Yu Ching-Han, Hsieh Yih-Shou
Аннотация
AIMS: 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.
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.