title: Difference in mechanism between glyceraldehyde- and glucose-induced insulin secretion from isolated rat pancreatic islets.
abstract: The effects of D-glyceraldehyde and glucose on islet function were compared in order to investigate the difference between them in the mechanism by which they induce insulin secretion. The stimulation of insulin secretion from isolated rat islets by 10 mM glyceraldehyde was not completely inhibited by either 150 microM diazoxide (an opener of ATP-sensitive K(+) channels) or 5 microM nitrendipine (an L-type Ca(2+)-channel blocker), whereas the stimulation of insulin secretion by 20 mM glucose was completely inhibited by either drug. The insulin secretion induced by glyceraldehyde was less augmented by 100 microM carbachol (a cholinergic agonist) than that induced by glucose. The stimulation of myo-inositol phosphate production by 100 microM carbachol was more marked in islets incubated with the hexose than with the triose. The content of glyceraldehyde 3-phosphate, a glycolytic intermediate, in islets incubated with glyceraldehyde was far higher than that in islets incubated with glucose, whereas the ATP content in islets incubated with the triose was significantly lower than that in islets incubated with the hexose. These results suggest that glyceraldehyde not only mimics the effect of glucose on insulin secretion but also has the ability to cause the secretion of insulin without the influx of Ca(2+ )through voltage-dependent Ca(2+) channels. The reason for the lower potency of the triose than the hexose in stimulating insulin secretion is also discussed.
authors.affiliation: Department of Pathobiochemistry, Faculty of Pharmacy, Meijo University, Tempaku-ku, Nagoya 468-8503, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Taniguchi
authors.forename: M
authors.initials: M
authors.lastname: Okinaka
authors.forename: K
authors.initials: K
authors.lastname: Tanigawa
authors.forename: I
authors.initials: I
authors.lastname: Miwa
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000494:pharmacology; D003981:Diazoxide / Q000494:pharmacology; D005260:Female; D005947:Glucose / Q000378:metabolism* / Q000494:pharmacology; D005985:Glyceraldehyde / Q000378:metabolism* / Q000494:pharmacology; D066298:In Vitro Techniques; D007295:Inositol Phosphates / Q000378:metabolism; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D019344:Lactic Acid / Q000378:metabolism; D009568:Nitrendipine / Q000494:pharmacology; D019289:Pyruvic Acid / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014305:Triose-Phosphate Isomerase / Q000187:drug effects / Q000378:metabolism
chemical_list: D002121:Calcium Channel Blockers; D018679:Cholinergic Agonists; D007295:Inositol Phosphates; D007328:Insulin; D019344:Lactic Acid; D005985:Glyceraldehyde; D019289:Pyruvic Acid; D000255:Adenosine Triphosphate; D002217:Carbachol; D009568:Nitrendipine; D014305:Triose-Phosphate Isomerase; D005947:Glucose; D003981:Diazoxide