Effects of Stanniocalcin-1 on glucose flux in rat brown adipose tissue

Publication date: Available online 20 April 2017
Source:Biochimie
Author(s): Aline G. Cozer, Márcia Trapp, Tiago L. Martins, Luciano Stürmer De Fraga, Claudia Vieira Marques, Jorge Felipe A. Model, Vanessa Schein, Luiz Carlos Kucharski, Roselis S.M. Da Silva
The present work assesses in vitro the role of human Stanniocalcin 1 (hSTC-1) in ¹⁴C-glucose metabolism in brown adipose tissue (BAT) from fed rat. In the fed state, hSTC-1 decreases the incorporation of ¹⁴C from glucose into lipids in the rat BAT. The data support the hypothesis that the capacity of the glycerol-3-phosphate (G3P)-generating pathway (glycolysis) from glucose is regulated by hSTC-1, decreasing the adequate supply of G3P needed for fatty acid esterification and triacylglycerol (TG) storage in BAT. The results also suggest the effect of hSTC-1 on de novo fatty acid synthesis from pyruvate generated by ¹⁴C-glucose in the glycolysis pathway. In addition, by decreasing lipogenesis, hSTC-1 increased ATP levels and these two factors may decrease BAT thermogenic function. The presence of hSTC-1 in the incubation medium did not alter ¹⁴C-glucose and ¹⁴C-1-palmitic acid oxidation. The uncoupling protein 1 (UCP-1) expression was not altered by hSTC-1 either. In conclusion, hSTC-1 is one of the hormonal factors that control glucose metabolism in BAT in the fed state. The decrease of TG capacity synthesis from ¹⁴C-glucose by hSTC-1 compromises the BAT thermogenic capacity. Furthermore, the increase in ATP levels would inhibit a futile cycle via UCP-1, which dissipates oxidative energy as heat.

Graphical abstract

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