Ghrelin differentially modulates glucose-induced insulin secretion according to feeding status in sheep.
Ghrelin differentially modulates glucose-induced insulin secretion according to feeding status in sheep.
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DOI：
10.1677/joe-07-0206
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发表时间：
2007-09
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影响因子：
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通讯作者：
Hideyuki Takahashi;Y. Kurose;M. Sakaida;Yoshihiro Suzuki;Shigeki Kobayashi;T. Sugino;M. Kojima;K. Kangawa;Y. Hasegawa;Y. Terashima
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文献类型：
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作者：
Hideyuki Takahashi;Y. Kurose;M. Sakaida;Yoshihiro Suzuki;Shigeki Kobayashi;T. Sugino;M. Kojima;K. Kangawa;Y. Hasegawa;Y. Terashima
本研究的目的是探讨生长素释放肽在绵羊禁食和进食状态下葡萄糖诱导的胰岛素分泌中的作用。阉割的萨福克公羊每天喂食一次苜蓿干草块的维持饮食。实验1和2分别在喂食后48至53小时（空腹状态）和3至8小时（进餐状态）进行高血糖钳夹（HGC）以检查葡萄糖诱导的胰岛素反应。在 HGC 开始后 0、60 和 120 分钟，静脉内施用总剂量为 70 nmol/kg 体重的 D-Lys3-GHRP6（一种 GH 促分泌素受体 1a (GHS-R1a) 拮抗剂）。在禁食状态下，生长素释放肽拮抗剂显着（P < 0.01）增强葡萄糖诱导的胰岛素分泌。在餐食状态下，静脉注射。给予合成羊生长素释放肽（HGC 期间每分钟 0.04 微克/公斤体重）显着（P < 0.05）增强葡萄糖诱导的胰岛素分泌。 d-Lys3-GHRP6 治疗抑制了 ghrelin 诱导的胰岛素分泌增强。总之，在空腹和进餐状态下，ghrelin 通过 GHS-R1a 分别对葡萄糖诱导的胰岛素分泌具有抑制和刺激作用。
The present study was conducted to investigate roles of ghrelin in glucose-induced insulin secretion in fasting- and meal-fed state in sheep. Castrated Suffolk rams were fed a maintenance diet of alfalfa hay cubes once a day. Hyperglycemic clamp (HGC) was carried out to examine glucose-induced insulin response from 48 to 53 h (fasting state) and from 3 to 8 h (meal-fed state) after feeding in Experiment 1 and 2 respectively. Total dose of 70 nmol/kg body weight of D-Lys3-GHRP6, a GH secretagogue receptor 1a (GHS-R1a) antagonist, was intravenously administered at 0, 60, and 120 min after the commencement of HGC. In the fasting state, the ghrelin antagonist significantly (P < 0.01) enhanced glucose-induced insulin secretion. In the meal-fed state, i.v. administration of synthetic ovine ghrelin (0.04 microg/kg body weight per min during HGC) significantly (P < 0.05) enhanced glucose-induced insulin secretion. d-Lys3-GHRP6 treatment suppressed ghrelin-induced enhancement of the insulin secretion. In conclusion, ghrelin has an inhibitory and stimulatory role in glucose-induced insulin secretion via GHS-R1a in fasting- and meal-fed state respectively.