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Titolo:
Carbachol restores insulin release in diabetic GK rat islets by mechanismslargely involving hydrolysis of diacylglycerol and direct interaction withthe exocytotic machinery
Autore:
Guenifi, A; Simonsson, E; Karlsson, S; Ahren, B; Abdel-Halim, SM;
Indirizzi:
Karolinska Inst, Dept Mol Med, Endocrine & Diabet Unit, Stockholm, Sweden Karolinska Inst Stockholm Sweden crine & Diabet Unit, Stockholm, Sweden Univ Lund, Dept Med, Malmo, Sweden Univ Lund Malmo SwedenUniv Lund, Dept Med, Malmo, Sweden
Titolo Testata:
PANCREAS
fascicolo: 2, volume: 22, anno: 2001,
pagine: 164 - 171
SICI:
0885-3177(200103)22:2<164:CRIRID>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; PANCREATIC-ISLETS; GLUCOSE-TOLERANCE; ADENYLYL-CYCLASE; PHOSPHOLIPASE-C; WISTAR RATS; SECRETION; STIMULATION; CAMP; MICE;
Keywords:
Goto-Kahizaki (GK) rats; insulin release; type II diabetes; PLC; phospholipase-C; carbachol;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Abdel-Halim, SM Karolinska Hosp, Dept Mol Med, Endocrine & Diabet Unit, S-17176 Stockholm,Sweden Karolinska Hosp Stockholm Sweden S-17176 tockholm,Sweden
Citazione:
A. Guenifi et al., "Carbachol restores insulin release in diabetic GK rat islets by mechanismslargely involving hydrolysis of diacylglycerol and direct interaction withthe exocytotic machinery", PANCREAS, 22(2), 2001, pp. 164-171

Abstract

In several models of insulin resistance, cholinergically induced insulin secretion is augmented. We studied here whether this also is present in the spontaneously diabetic GK (Goto-Kakizaki) rat pancreas. Using carbachol (50mu mol/L), enhanced insulin release was elicited in perfused pancreas under normal or depolarized conditions in GK compared with control rats at 3.3 mmol/L glucose (p < 0.03). Carbachol fully normalized insulin secretion in GK rats at 16.7 mmol/L glucose through an effect abolished by atropine. Similarly, direct stimulation of protein kinase C (PKC) with the DAG-permeablecompound 1-oleoyl-2-acetyl-sn-glycerol (OAG, 300 <mu>mol/L) induced more pronounced insulin release in GK islets than in control islets. The diacylglycerol (DAG) lipase inhibitor RHC-80267 (35 mu mol/L) significantly reducedcarbachol effects in control and GK islets, but had no effect on GAG-induced insulin release. The enhanced insulinotropic effects of carbachol in GK islets was not accompanied by increased cyclic adenosine monophosphate (cAMP) or arachidonic acid (AA) formation in GK when compared with control islets, In conclusion, cholinergic stimulation induced enhanced insulin releasein diabetic GK islets. This is largely mediated through mechanisms involving hydrolysis of DAG to AA and interaction with exocytotic steps of insulinrelease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 07:33:31