Taurine supplementation: involvement of cholinergic/phospholipase C and protein kinase A pathways in potentiation of insulin secretion and Ca2+ handling in mouse pancreatic islets

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 k...

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Published inBritish journal of nutrition Vol. 104; no. 8; pp. 1148 - 1155
Main Authors Ribeiro, Rosane A., Vanzela, Emerielle C., Oliveira, Camila A. M., Bonfleur, Maria L., Boschero, Antonio C., Carneiro, Everardo M.
Format Journal Article
LanguageEnglish
Published Cambridge, UK Cambridge University Press 28.10.2010
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Summary: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 PLCβ2 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.
Bibliography:http://dx.doi.org/10.1017/S0007114510001820
ark:/67375/6GQ-VR179QSW-8
ArticleID:00182
PII:S0007114510001820
istex:6C8E76AEA610AD0863FEECEBBA0F638F3B6E3514
Abbreviations: Cch, carbachol; CTL, control; EGTA, ethylene glycol tetraacetic acid; F340:F380, fluorescence ratio at 340 and 380 nm; H89, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline sulfonamide; IBMX, 3-isobutyl-1-methyl-xanthine; IP3, inositol-1,4,5-trisphosphate; KRB, Krebs–Ringer bicarbonate; PK, protein kinase; PKI, protein kinase inhibitor-(6–22)-amide; PMA, phorbol 12-myristate 13-acetate; TAU, taurine
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0007-1145
1475-2662
DOI:10.1017/S0007114510001820