{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:20:09Z","timestamp":1784557209504,"version":"3.55.0"},"reference-count":33,"publisher":"Bioscientifica","issue":"1","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2013,7]]},"abstract":"\n Glucose-induced insulin secretion from pancreatic \u03b2-cells critically depends on the activity of ATP-sensitive K\n +<\/jats:sup>\n channels (K\n ATP<\/jats:sub>\n channel). We previously generated mice lacking\n Kir6.2<\/jats:italic>\n , the pore subunit of the \u03b2-cell K\n ATP<\/jats:sub>\n channel (\n Kir6.2<\/jats:italic>\n \n \u2212\/\u2212<\/jats:italic>\n <\/jats:sup>\n ), that show almost no insulin secretion in response to glucose\n in vitro<\/jats:italic>\n . 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 (\n Kir6.2<\/jats:italic>\n \n +<\/jats:italic>\n <\/jats:sup>\n \n \/<\/jats:italic>\n <\/jats:sup>\n \n +<\/jats:italic>\n <\/jats:sup>\n ) and\n Kir6.2<\/jats:italic>\n \n \u2212\/\u2212<\/jats:italic>\n <\/jats:sup>\n mice. Under\n ad libitum<\/jats:italic>\n feeding or during voluntary feeding of standard chow, blood glucose levels and plasma insulin levels were similar in\n Kir6.2<\/jats:italic>\n \n +<\/jats:italic>\n <\/jats:sup>\n \n \/<\/jats:italic>\n <\/jats:sup>\n \n +<\/jats:italic>\n <\/jats:sup>\n and\n Kir6.2<\/jats:italic>\n \n \u2212\/\u2212<\/jats:italic>\n <\/jats:sup>\n mice. By voluntary feeding of carbohydrate alone, insulin secretion was induced significantly in\n Kir6.2<\/jats:italic>\n \n \u2212\/\u2212<\/jats:italic>\n <\/jats:sup>\n mice but was markedly attenuated compared with that in\n Kir6.2<\/jats:italic>\n \n +<\/jats:italic>\n <\/jats:sup>\n \n \/<\/jats:italic>\n <\/jats:sup>\n \n +<\/jats:italic>\n <\/jats:sup>\n mice. On forced feeding of standard chow or carbohydrate alone, the insulin secretory response was markedly impaired or completely absent in\n Kir6.2<\/jats:italic>\n \n \u2212\/\u2212<\/jats:italic>\n <\/jats:sup>\n mice. Pretreatment with a muscarine receptor antagonist, atropine methyl nitrate, which does not cross the blood\u2013brain barrier, almost completely blocked insulin secretion induced by voluntary feeding of standard chow or carbohydrate in\n Kir6.2<\/jats:italic>\n \n \u2212\/\u2212<\/jats:italic>\n <\/jats:sup>\n mice. Substantial glucose-induced insulin secretion was induced in the pancreas perfusion study of\n Kir6.2<\/jats:italic>\n \n \u2212\/\u2212<\/jats:italic>\n <\/jats:sup>\n mice only in the presence of carbamylcholine. These results suggest that a K\n ATP<\/jats:sub>\n channel-independent mechanism mediated by the vagal nerve plays a critical role in insulin secretion in response to nutrients\n in vivo<\/jats:italic>\n .\n <\/jats:p>","DOI":"10.1530\/joe-12-0579","type":"journal-article","created":{"date-parts":[[2013,4,23]],"date-time":"2013-04-23T04:31:21Z","timestamp":1366691481000},"page":"25-33","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":12,"title":["Cephalic phase insulin secretion is KATP channel 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