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Metabolism and Regulation of Food Intake

開催日 2014/9/13
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Glucose, insulin and CCK activate nesfatin-1 neurons in the hypothalamic paraventricular nucleus

  • P3-196
  • Darambazar Gantulga:1 Yuko Maejima:2 Masanori Nakata:2 Toshihiko Yada:2,3 
  • 1:Dept of Biol and Histology, Sch of Biomedicine, Health Sciences Univ, Ulaanbaatar, Mongolia 2:Dept. of Physiol., Jichi Med. Univ., Shimotsuke, Japan 3:Dept. of Developmental Physiology, Div. of Adaptation Develop., Natl. Inst. for Physiological Sci., Okazaki, Japan 

Nesfatin-1, a recently discovered anorectic peptide processed from NUCB2, is expressed in the neurons in specific brain areas including the paraventricular nucleus of hypothalamus (PVN), a pivotal center of feeding regulation. The regulation of nesfatin-1 expressing neurons in the PVN has little been studied. Since starvation decreases and refeeding stimulates nesfatin-1 expression specifically in the PVN, we examined direct effects of meal-evoked metabolic factors, glucose, insulin and cholecystokinin (CCK), on PVN nesfatin-1 neurons.

We isolated single neurons from PVN and measured cytosolic calcium concentration ([Ca2+]i) by ratiometric fura-2 fluorescence imaging.

Glucose (10 mM), insulin (10-13M) and CCK (10-13M) induced increases in [Ca2+]i in 55 of 311 (16.6%), 32 of 249 (12.9%) and 8 of 39 (20.5%) PVN neurons tested, respectively. Moreover, the post [Ca2+]i measurement immunocytochemistry identified 58% of glucose-responsive neurons, 63% of insulin-responsive neurons, and 50% of CCK-responsive neurons as nesfatin-1 neurons, indicating that nesfatin-1 neuron is the major target for glucose, insulin and CCK in the PVN. Intracerebroventricular injection of CCK (30 pmol) significantly increased mRNA expression of nesfatin-1 in the PVN and inhibited feeding. In addition, antiserum against nesfatin-1 blocked CCK-induced anorexia.

These results demonstrate that glucose, insulin and CCK directly interact with and increase [Ca2+]i in PVN nesfatin-1 neurons, and that the nesfatin-1 neuron is the major target for all of them in the PVN. Postprandial activation of the PVN nesfatin-1 neurons could be mediated by these meal-evoked nutritional and endocrine factors, which potentially contributes to generation of satiety.

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