Kim Jongwan, Yun Eun-Young, Quan Fu-Shi, Park Seung-Won, Goo Tae-Won
Department of Anatomy, Graduate School of Dongguk University College of Medicine, 123 Dongdae-ro, Gyeongju-si 38066, Republic of Korea.
Graduate School of Integrated Bioindustry, Sejong University, 209 Neungdong-ro, Gwangjin-gu, Seoul 05006, Republic of Korea.
Evid Based Complement Alternat Med. 2017;2017:3607089. doi: 10.1155/2017/3607089. Epub 2017 Jul 17.
The -glucosidase inhibitor, 1-deoxynojirimycin (DNJ), is widely used for its antiobesity and antidiabetic effects. Researchers have demonstrated that DNJ regulates body weight by increasing adiponectin levels, which affects energy intake and prevents diet-induced obesity. However, the mechanism by which centrally administered DNJ exerts anorexigenic effects has not been studied until now. We investigated the effect of DNJ in the hypothalamus of mice with high-fat diet-induced obesity. Results showed that intracerebroventricular (ICV) administration of DNJ reduced hypothalamic ER stress, which activated the leptin-induced Janus-activated kinase 2 (JAK2)/signal transducers and activators of transcription 3 (STAT3) signaling pathway to cause appetite suppression. We conclude that DNJ may reduce obesity by moderating feeding behavior and ER stress in the hypothalamic portion of the central nervous system (CNS).
α-葡萄糖苷酶抑制剂1-脱氧野尻霉素（DNJ）因其抗肥胖和抗糖尿病作用而被广泛使用。研究人员已证明，DNJ通过提高脂联素水平来调节体重，脂联素会影响能量摄入并预防饮食诱导的肥胖。然而，迄今为止，中枢给予DNJ产生厌食作用的机制尚未得到研究。我们研究了DNJ对高脂饮食诱导肥胖小鼠下丘脑的影响。结果显示，脑室内（ICV）给予DNJ可减轻下丘脑内质网应激，从而激活瘦素诱导的Janus激活激酶2（JAK2）/信号转导子和转录激活子3（STAT3）信号通路，进而导致食欲抑制。我们得出结论，DNJ可能通过调节中枢神经系统（CNS）下丘脑部分的摄食行为和内质网应激来减轻肥胖。
