title: Taurine supplementation increases K(ATP) channel protein content, improving Ca2+ handling and insulin secretion in islets from malnourished mice fed on a high-fat diet.
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 Ca(2+) 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.
authors.affiliation: Laboratório de Pâncreas Endócrino e Metabolismo, Departamento de Biologia Estrutural e Funcional, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), Campinas, SP, Brazil.
authors.forename: Jean F
authors.initials: JF
authors.lastname: Vettorazzi
authors.forename: Rosane A
authors.initials: RA
authors.lastname: Ribeiro
authors.forename: Junia C
authors.initials: JC
authors.lastname: Santos-Silva
authors.forename: Patricia C
authors.initials: PC
authors.lastname: Borck
authors.forename: Thiago M
authors.initials: TM
authors.lastname: Batista
authors.forename: Tarlliza R
authors.initials: TR
authors.lastname: Nardelli
authors.forename: Antonio C
authors.initials: AC
authors.lastname: Boschero
authors.forename: Everardo M
authors.initials: EM
authors.lastname: Carneiro
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004041:Dietary Fats / Q000494:pharmacology*; D019587:Dietary Supplements; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism*; D008297:Male; D044342:Malnutrition / Q000378:metabolism*; D051379:Mice; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D050825:Synaptosomal-Associated Protein 25 / Q000378:metabolism; D013654:Taurine / Q000494:pharmacology*; D000099161:Kcnj11 Channel
chemical_list: D002118:Calcium; D004041:Dietary Fats; D007328:Insulin; D024661:Potassium Channels, Inwardly Rectifying; D050825:Synaptosomal-Associated Protein 25; D013654:Taurine; D000099161:Kcnj11 Channel; C494209:Snap25 protein, mouse