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中枢前列腺素D2通过小鼠中的神经肽Y系统刺激食物摄入。

Central prostaglandin D(2) stimulates food intake via the neuropeptide Y system in mice.

作者信息

Ohinata Kousaku, Takagi Kuniko, Biyajima Kyoko, Fujiwara Yoko, Fukumoto Shingo, Eguchi Naomi, Urade Yoshihiro, Asakawa Akihiro, Fujimiya Mineko, Inui Akio, Yoshikawa Masaaki

机构信息

Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Gokasho Uji, Kyoto, Japan.

出版信息

FEBS Lett. 2008 Mar 5;582(5):679-84. doi: 10.1016/j.febslet.2008.01.050. Epub 2008 Feb 5.

Abstract

We found that prostaglandin (PG) D(2), the most abundant PG in the central nervous system, stimulates food intake after intracerebroventricular administration in mice. The orexigenic effect of PGD(2) was mimicked by a selective agonist for the DP(1) receptor among two receptor subtypes for PGD(2), and abolished by its antagonist. Central administration of an antagonist or antisense oligodeoxynucleotide for the DP(1) receptor remarkably decreased food intake, body weight and fat mass. Hypothalamic mRNA levels of lipocalin-type PGD synthase were up-regulated after fasting. The orexigenic activity of PGD(2) was also abolished by an antagonist for neuropeptide Y (NPY) Y(1) receptor. Taken together, PGD(2) may stimulate food intake through central DP(1) receptor coupled to the NPY system.

摘要

我们发现,前列腺素(PG)D2是中枢神经系统中含量最丰富的前列腺素,在小鼠脑室内注射后会刺激食物摄入。在PGD2的两种受体亚型中,DP1受体的选择性激动剂可模拟PGD2的促食欲作用,而其拮抗剂可消除该作用。对DP1受体给予拮抗剂或反义寡脱氧核苷酸进行中枢给药,可显著降低食物摄入量、体重和脂肪量。禁食后,下丘脑脂质运载蛋白型PGD合酶的mRNA水平上调。神经肽Y(NPY)Y1受体的拮抗剂也可消除PGD2的促食欲活性。综上所述,PGD2可能通过与NPY系统偶联的中枢DP1受体刺激食物摄入。

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