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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
Ribeiro, Rosane A. [1] ; Vanzela, Emerielle C. [1] ; Oliveira, Camila A. M. [1] ; Bonfleur, Maria L. [1] ; Boschero, Antonio C. [1] ; Carneiro, Everardo M. [1]
Total Authors: 6
Affiliation:
[1] Univ Estadual Campinas UNICAMP, Inst Biol, Dept Anat Biol Celular & Fisiol & Biofis, Campinas, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: BRITISH JOURNAL OF NUTRITION; v. 104, n. 8, p. 1148-1155, OCT 2010.
Web of Science Citations: 39
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 Ca(2+) 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 mu M-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 Ca(2+) mobilisation and PLC(beta 2) protein expression. The Ca(2+) 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 PKA alpha protein. This protein may play a role in cation accumulation, since the amount of Ca(2+) 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 Ca(2+), and these effects seem to involve the activation of both PLC-inositol-1,4,5-trisphosphate and cAMP-PKA pathways. (AU)

FAPESP's process: 07/50365-4 - Study of the destruction mechanisms of beta pancreatic cells during the onset of Diabetes Mellitus (DM2): search for inhibition strategies of this process as well as for the recovery of insular mass in different animal models
Grantee:Antonio Carlos Boschiero
Support Opportunities: Research Projects - Thematic Grants