한빛사 논문
Abstract
Yu Mi Han1, Gil Myoung Kang1, Kyunghee Byun2, Hyuk Wan Ko3, Joon Kim4, Mi-Seon Shin5, Hyun-Kyong Kim1, So Young Gil1, Ji Hee Yu5, Bonghee Lee2,* and Min-Seon Kim1,5,*
1Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea.
2Lee Gil Ya Cancer and Diabetes Institute, Gachon University of Medicine and Science, Incheon, Republic of Korea.
3College of Pharmacy, Dongguk University, Goyangsi, Gyeonggido, Republic of Korea.
4Graduate School of Medical Science and Engineering, KAIST, Daejeon, Republic of Korea.
5Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Authorship note: Yu Mi Han and Gil Myoung Kang contributed equally to this work.
*Address correspondence to: Min-Seon Kim, Appetite Regulation Laboratory, Asan Institute for Life Sciences, Division of Endocrinology and Metabolism, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul 138-736, Republic of Korea. Or to: Bonghee Lee, Center for Genomics and Proteomics, Lee Gil Ya Cancer and Diabetes Institute, Gachon University of Medicine and Science, Incheon 406-840, Republic of Korea.
The majority of mammalian cells have nonmotile primary cilia on their surface that act as antenna-like sensory organelles. Genetic defects that result in ciliary dysfunction are associated with obesity in humans and rodents, which suggests that functional cilia are important for controlling energy balance. Here we demonstrated that neuronal cilia lengths were selectively reduced in hypothalami of obese mice with leptin deficiency and leptin resistance. Treatment of N1 hypothalamic neuron cells with leptin stimulated cilia assembly via inhibition of the tumor suppressors PTEN and glycogen synthase kinase 3β (GSK3β). Induction of short cilia in the hypothalamus of adult mice increased food intake and decreased energy expenditure, leading to a positive energy balance. Moreover, mice with short hypothalamic cilia exhibited attenuated anorectic responses to leptin, insulin, and glucose, which indicates that leptin-induced cilia assembly is essential for sensing these satiety signals by hypothalamic neurons. These data suggest that leptin governs the sensitivity of hypothalamic neurons to metabolic signals by controlling the length of the cell’s antenna.
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