Ghrelin raises [Ca2+]i via AMPK in hypothalamic arcuate nucleus NPY neurons |
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Authors: | Kohno Daisuke Sone Hideyuki Minokoshi Yasuhiko Yada Toshihiko |
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Affiliation: | a Division of Integrative Physiology, Department of Physiology, Jichi Medical University, School of Medicine, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan b Department of Human Life and Environmental Science, Niigata Women’s College, Ebigase, Niigata 950-8680, Japan c Division of Endocrinology and Metabolism, Department of Developmental Physiology, National Institute for Physiological Sciences, 38 Nishigonaka, Myodaiji, Okazaki, Aichi 444-8585, Japan |
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Abstract: | Ghrelin, an orexigenic hormone, directly activates neuropeptide (NPY) neurons in the hypothalamic arcuate nucleus (ARC), and thereby stimulates food intake. The hypothalamic level of AMP-activated protein kinase (AMPK), an intracellular energy sensor, is activated by peripheral and central administration of ghrelin. We examined whether ghrelin regulates AMPK activity in NPY neurons of the ARC. Single neurons were isolated from the ARC and cytosolic Ca2+ concentration ([Ca2+]i) was measured by fura-2 microfluorometry, followed by immunocytochemical identification of NPY, phospho-AMPK, and phospho-acetyl-CoA carboxylase (ACC). Ghrelin and AICAR, an AMPK activator, increased [Ca2+]i in neurons isolated from the ARC. The ghrelin-responsive neurons highly overlapped with AICAR-responsive neurons. The neurons that responded to both ghrelin and AICAR were primarily NPY-immunoreactive neurons. Treatment with ghrelin increased phosphorylation of AMPK and ACC. An AMPK inhibitor, compound C, suppressed ghrelin-induced [Ca2+]i increases. These results demonstrate that ghrelin increases [Ca2+]i via AMPK-mediated signaling in the ARC NPY neurons. |
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Keywords: | AMPK NPY Ghrelin ACC Ca2+ AICAR Compound C Feeding Arcuate nucleus |
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