Taurine supplementation: involvement of cholinergic/phospholipase C and protein kinase A pathways in potentiation of insulin secretion and Ca2+ handling in mouse pancreatic islets.
Br J Nutr
; 104(8): 1148-55, 2010 Oct.
Article
en En
| MEDLINE
| ID: mdl-20591207
ABSTRACT
Taurine (TAU) supplementation increases insulin secretion in response to high glucose concentrations in rodent islets. This effect is probably due to an increase in Ca2+ handling by the islet cells. Here, we investigated the possible involvement of the cholinergic/phospholipase C (PLC) and protein kinase (PK) A pathways in this process. Adult mice were fed with 2% TAU in drinking water for 30 d. The mice were killed and pancreatic islets isolated by the collagenase method. Islets from TAU-supplemented mice showed higher insulin secretion in the presence of 8.3 mm-glucose, 100 µm-carbachol (Cch) and 1 mm-3-isobutyl-1-methyl-xanthine (IBMX), respectively. The increase in insulin secretion in response to Cch in TAU islets was accompanied by a higher intracellular Ca2+ mobilisation and PLCß2 protein expression. The Ca2+ uptake was higher in TAU islets in the presence of 8.3 mm-glucose, but similar when the islets were challenged by glucose plus IBMX. TAU islets also showed an increase in the expression of PKAα protein. This protein may play a role in cation accumulation, since the amount of Ca2+ in these islets was significantly reduced by the PKA inhibitors N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline sulfonamide (H89) and PK inhibitor-(6-22)-amide (PKI). In conclusion, TAU supplementation increases insulin secretion in response to glucose, favouring both influx and internal mobilisation of Ca2+, and these effects seem to involve the activation of both PLC-inositol-1,4,5-trisphosphate and cAMP-PKA pathways.
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Taurina
/
Calcio
/
Islotes Pancreáticos
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Proteínas Quinasas Dependientes de AMP Cíclico
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Fosfolipasa C beta
/
Insulina
Límite:
Animals
Idioma:
En
Revista:
Br J Nutr
Año:
2010
Tipo del documento:
Article
País de afiliación:
Brasil