The present work assesses in vitro the role of human Stanniocalcin 1 (hSTC-1) in C-glucose metabolism in brown adipose tissue (BAT) from fed rat. In the fed state, hSTC-1 decreases the incorporation ofC 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 C-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 alterC-glucose and C-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 fromC-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.
The present work assesses in vitro the role of human Stanniocalcin 1 (hSTC-1) in glucose metabolism in white retroperitoneal adipose tissue (WRAT) from fed rat. In the fed state, hSTC1 increases the incorporation of C from glucose into lipids in the rat WRAT. The increase in lipogenesis capacity supports the hypothesis that the activity of the glycerol-3-phosphate-generating pathway (glycolysis) from glucose is regulated by hSTC-1. The effect of hSTC-1 on de novo fatty acid synthesis and on glucose oxidation in WRAT is supported by an 85 % increase inCO production from C-glucose. The incubation of WRAT in the presence of hSTC-1 maintained the ADP/ATP ratio close to the control group. The presence of hSTC-1 in the incubation medium did not inhibit the lipolytic effect of epinephrine. In conclusion, hSTC-1 is one of the hormonal factors that control glucose metabolism in WRAT in the fed state.
Dehydroepiandrosterone (DHEA) is a steroid hormone that presents several effects on metabolism; however, most of the studies have been performed on male animals, while few authors have investigated possible sex differences regarding the metabolic effects of DHEA. Therefore, the aim of this study was to evaluate the effect of different doses of DHEA on metabolic parameters of male and ovariectomized female Wistar rats. Sex differences were found in the metabolism of distinct substrates and in relation to the effect of DHEA. In respect to the glucose metabolism in the liver, the conversion of glucose to CO and the synthesis of lipids from glucose were 53% and 33% higher, respectively, in males. Also, DHEA decreased hepatic lipogenesis only in females. Regarding the hepatic glycogen synthesis pathway, females presented 73% higher synthesis than males, and the effect of DHEA was observed only in females, where it decreased this parameter. In the adipose tissue, glucose uptake was 208% higher in females and DHEA decreased this parameter. In the muscle, glucose uptake was 168% higher in females and no DHEA effect was observed. In summary, males and females present a different metabolic profile, with females being more susceptible to the metabolic effects of DHEA.
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