Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/85782
Type: Artigo de periódico
Title: Taurine Supplementation Increases Katp Channel Protein Content, Improving Ca2+ Handling And Insulin Secretion In Islets From Malnourished Mice Fed On A High-fat Diet
Author: Vettorazzi J.F.
Ribeiro R.A.
Santos-Silva J.C.
Borck P.C.
Batista T.M.
Nardelli T.R.
Boschero A.C.
Carneiro E.M.
Abstract: Pancreatic β-cells are highly sensitive to suboptimal or excess nutrients, as occurs in protein-malnutrition and obesity. Taurine (Tau) improves insulin secretion in response to nutrients and depolarizing agents. Here, we assessed the expression and function of Cav and KATP channels in islets from malnourished mice fed on a high-fat diet (HFD) and supplemented with Tau. Weaned mice received a normal (C) or a low-protein diet (R) for 6 weeks. Half of each group were fed a HFD for 8 weeks without (CH, RH) or with 5 % Tau since weaning (CHT, RHT). Isolated islets from R mice showed lower insulin release with glucose and depolarizing stimuli. In CH islets, insulin secretion was increased and this was associated with enhanced KATP inhibition and Cav activity. RH islets secreted less insulin at high K+ concentration and showed enhanced KATP activity. Tau supplementation normalized K+-induced secretion and enhanced glucose-induced Ca 2+ influx in RHT islets. R islets presented lower Ca2+ influx in response to tolbutamide, and higher protein content and activity of the Kir6.2 subunit of the KATP. Tau increased the protein content of the α1.2 subunit of the Cav channels and the SNARE proteins SNAP-25 and Synt-1 in CHT islets, whereas in RHT, Kir6.2 and Synt-1 proteins were increased. In conclusion, impaired islet function in R islets is related to higher content and activity of the KATP channels. Tau treatment enhanced RHT islet secretory capacity by improving the protein expression and inhibition of the KATP channels and enhancing Synt-1 islet content. © 2014 Springer-Verlag.
Editor: Springer-Verlag Wien
Rights: fechado
Identifier DOI: 10.1007/s00726-014-1763-6
Address: http://www.scopus.com/inward/record.url?eid=2-s2.0-84906323842&partnerID=40&md5=a3748605f030f25d867f907f1edd0678
Date Issue: 2014
Appears in Collections:Unicamp - Artigos e Outros Documentos

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