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

- hSTC-1 inhibited lipid synthesis from 14C-glucose in rat brown tissue (BAT).
- hSTC-1 increased ATP concentration but did not alter ADP/ATP ratio in BAT.
- hSTC-1 did not change glucose or fatty acid oxidation in BAT.
- hSTC-1 did not change UCP-1 expression in BAT.

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.

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