Proceedings of Annual Meeting of the Physiological Society of Japan
Proceedings of Annual Meeting of the Physiological Society of Japan
Session ID : 2SG19-5
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Mechanisms and (patho)physiological roles of glucose monitoring by NPY neurons in the hypothalamic arcuate nucleus.
*Toshihiko YadaHideharu KuritaHumihiko MaekawaDaisuke KohnoYuko Maejima
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Abstract
Lowering glucose concentrations from 5-10 mM to 1-3 mM increased cytosolic Ca2+ concentration ([Ca2+]i) in 20% of isolated neurons from the rat hypothalamic arcuate nucleus (ARC), exhibiting the property of glucose-sensitive (GS) neurons. More than 90% of these GS neurons were neuropeptide Y (NPY)-containing neurons. In ARC GS neurons, low glucose-induced ([Ca2+]i) increases were mimicked by a non-metabolizable glucose analogue 2-deoxy-glucose, a glucokinase inhibitor mannoheptulose, and a mitochondrial inhibitor KCN. Furthermore, low glucose-induced ([Ca2+]i) increases were inhibited by blockers of L- and N-type Ca2+ channel blockers. These results indicate that changes in extracellular glucose concentrations are transduced to intracellular changes in glucose metabolism and energy production, which eventually stimulate Ca2+ influx through voltage-dependent Ca2+ channels. The coupling mechanisms between reduced energy state and Ca2+ channel activation remain to be elucidated. Intracerebroventricular injection of 2-deoxy-glucose and a glucokinase inhibitor, as well as NPY, enhanced food intake in rats. Fasting increased NPY mRNA level in ARC. Overexpression of NPY mRNA in ARC accounted for hyperphasia in the young-adult Goto-Kakizaki rats, a type 2 diabetic model. These results support physiological relevance of GS-NPY neurons in the regulation of feeding. [J Physiol Sci. 2007;57 Suppl:S33]
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© 2007 The Physiological Society of Japan
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