Taurine supplementation increases KATP channel protein content, improving Ca 2+ handling and insulin secretion in islets from malnourished mice fed on a high-fat diet
2014
Vettorazzi, Jean F. | Ribeiro, Rosane A. | Santos-Silva, Junia C. | Borck, Patricia C. | Batista, Thiago M. | Nardelli, Tarlliza R. | Boschero, Antonio C. | Carneiro, Everardo M.
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 KATPchannels 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 KATPinhibition and Cav activity. RH islets secreted less insulin at high K⁺concentration and showed enhanced KATPactivity. Tau supplementation normalized K⁺-induced secretion and enhanced glucose-induced Ca²⁺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 KATPchannels. Tau treatment enhanced RHT islet secretory capacity by improving the protein expression and inhibition of the KATPchannels and enhancing Synt-1 islet content.
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