Cephalic phase insulin secretion is KATP channel independent

Yusuke Seino, Takashi Miki, Wakako Fujimoto, Eun Young Lee, Yoshihisa Takahashi, Kohtaro Minami, Yutaka Oiso, Susumu Seino

研究成果: Article査読

11 被引用数 (Scopus)

抄録

Glucose-induced insulin secretion from pancreatic β-cells critically depends on the activity of ATP-sensitive K+ channels (KATP channel). We previously generated mice lacking Kir6.2, the pore subunit of the β-cell KATP channel (Kir6.2-/-), that show almost no insulin secretion in response to glucose in vitro. In this study, we compared insulin secretion by voluntary feeding (self-motivated, oral nutrient ingestion) and by forced feeding (intra-gastric nutrient injection via gavage) in wild-type (Kir6.2+/+) and Kir6.2-/- mice. Under ad libitum feeding or during voluntary feeding of standard chow, blood glucose levels and plasma insulin levels were similar in Kir6.2+/+ and Kir6.2-/- mice. By voluntary feeding of carbohydrate alone, insulin secretion was induced significantly in Kir6.2-/- mice but was markedly attenuated compared with that in Kir6.2+/+ mice. On forced feeding of standard chow or carbohydrate alone, the insulin secretory response was markedly impaired or completely absent in Kir6.2-/- mice. Pretreatment with a muscarine receptor antagonist, atropine methyl nitrate, which does not cross the blood-brain barrier, almost completely blocked insulin secretion induced by voluntary feeding of standard chow or carbohydrate in Kir6.2-/- mice. Substantial glucose-induced insulin secretion was induced in the pancreas perfusion study of Kir6.2-/- mice only in the presence of carbamylcholine. These results suggest that a KATP channel-independent mechanism mediated by the vagal nerve plays a critical role in insulin secretion in response to nutrients in vivo.

本文言語English
ページ(範囲)25-33
ページ数9
ジャーナルJournal of Endocrinology
218
1
DOI
出版ステータスPublished - 2013
外部発表はい

All Science Journal Classification (ASJC) codes

  • 内分泌学、糖尿病および代謝内科学
  • 内分泌学

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