Taurine (TAU) restores β-cell function in obesity; however, its action is lost in malnourished obese rodents. Here, we investigated the mechanisms involved in the lack of effects of TAU in this model. C57BL/6 mice were fed a control diet (CD) (14% protein) or a protein-restricted diet (RD) (6% protein) for 6 wk. Afterward, mice received a high-fat diet (HFD) for 8 wk [CD + HFD (CH) and RD + HFD (RH)] with or without 5% TAU supplementation after weaning on their drinking water [CH + taurine (CHT) and RH + taurine (RHT)]. The HFD increased insulin secretion through mitochondrial metabolism in CH and RH. TAU prevented all those alterations in CHT only. The expression of the taurine transporter (Tau-T), as well as TAU content in pancreatic islets, was increased in CH but had no effect on RH. Protein malnutrition programs β-cells and impairs TAU-induced restoration of mitochondrial metabolism and biogenesis. This may be associated with modulation of the expression of Tau-T in pancreatic islets, which may be responsible for the absence of effect of TAU in protein-malnourished obese mice.—Branco, R. C. S., Camargo, R. L., Batista, T. M., Vettorazzi, J. F., Borck, P. C., dos Santos-Silva, J. C. R., Boschero, A. C., Zoppi, C. C., Carneiro, E. M. Protein malnutrition blunts the increment of taurine transporter expression by a high-fat diet and impairs taurine reestablishment of insulin secretion.
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