title: Importance of nonionic signals for glucose-induced biphasic insulin secretion.
abstract: Glucose induces biphasic insulin secretion by the islet beta-cell. Based on recent knowledge on glucose signaling in the beta-cell, the underlying mechanisms for this biphasicity could be envisaged as follows. Glucose-induced elevation of cytosolic free Ca(2+) concentration, which is due to the electrophysiological events that originate in closure of the ATP-sensitive K(+) (K(ATP)) channel, most likely triggers the first phase. The second phase is produced by gradual augmentation and potentiation of Ca(2+)-triggered insulin release by the K(ATP) channel-independent, nonionic signals. Protein acylation may be involved in the nonionic signaling. In patients lacking functional K(ATP) channels, however, the first phase of glucose-induced insulin secretion is clearly retained, casting doubt on the simplistic view outlined above. In this pathological condition, the K(ATP) channel-independent, most likely nonionic, glucose action alone is sufficient for the first-phase response.
authors.affiliation: Department of Aging Medicine and Geriatrics, Shinshu University School of Medicine, Matsumoto, Japan. traizawa@hsp.md.shinshu-u.ac.jp
authors.forename: Toru
authors.initials: T
authors.lastname: Aizawa
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Sato
authors.forename: Mitsuhisa
authors.initials: M
authors.lastname: Komatsu
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D015221:Potassium Channels / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D007328:Insulin; D015221:Potassium Channels; D000255:Adenosine Triphosphate; D005947:Glucose