日本生理学会大会発表要旨集
日本生理学会大会発表要旨集
セッションID: 1P2-160
会議情報
オキシトシン受容体遺伝子欠損マウスは熱産生能が低下する
*笠原 好之高柳 友紀河田 照雄井樋 慶一西森 克彦
著者情報
キーワード: oxytocin, knockout, thermogenesis
会議録・要旨集 フリー

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抄録
We studied the physiological functions of oxytocin receptor (OXTR) in energy homeostasis using OXTR deficient (oxtr-/-) mice, that we recently generated by genetic engineering.Male oxtr-/- mice developed obesity by 13-week-old. Histrogical analysis of adipose tissue in male oxtr-/- mice showed lipid accumulation in gonadal white adipose tissue (WAT), and most of cells in brown adipose tissue (BAT) were filled with large lipid droplets, suggesting a typical feature in dysfunction of thermogenesis.When oxtr-/- mice were exposed to cold, their rectal temperature rapidly dropped.In oxtr-/- mice, UCP1 expressed in BAT was increased normaly by cold exposure, but the ratio of expressions of α2 to β3 adrenergic receptors (ARs) was altered in comparison with that in wildtype animals. Since these ARs were known to have opposite effects on thermoregulation, the inbalance of ARs might cause this dysfunction.We predicted that OXT/OXTR systems act thermoregulation via central nervous or hormonal systems because both OXT and OXTR were not expressed in mature brown adipocyte, and analysed OXT mRNA expressions in thermogenic ceter of hypothalamus, but no alterations were observed after cold exposure.We further study about the thermoregulatory system controlled by OXT and OXTR. [J Physiol Sci. 2006;56 Suppl:S230]
著者関連情報
© 2006 日本生理学会
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