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

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.

Stanniocalcin 1 Enhances Carbon Flux from Glucose to Lipids in White Retroperitoneal Adipose Tissue in the Fed Rat.

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 14C 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 in 14CO2 production from 14C-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.

Dietary n-3 long-chain polyunsaturated fatty acids modify phosphoenolpyruvate carboxykinase activity and lipid synthesis from glucose in adipose tissue of rats fed a high-sucrose diet.

Long-chain polyunsaturated n-3 fatty acids (n-3 LCPUFAs) have hypolipidemic effects and modulate intermediary metabolism to prevent or reverse insulin resistance in a way that is not completely elucidated. Here, effects of these fatty acids on the lipid profile, phosphoenolpyruvate carboxykinase (PEPCK) activity, lipid synthesis from glucose in epididymal adipose tissue (Ep-AT) and liver were investigated. Male rats were fed a high-sucrose diet (SU diet), containing either sunflower oil or a mixture of sunflower and fish oil (SU-FO diet), and the control group was fed a standard diet. After 13 weeks, liver, adipose tissue and blood were harvested and analysed. The dietary n-3 LCPUFAs prevented sucrose-induced increase in adiposity and serum free fat acids, serum and hepatic triacylglycerol and insulin levels. Furthermore, these n-3 LCPUFAs decreased lipid synthesis from glucose and increased PEPCK activity in the Ep-AT of rats fed the SU-FO diet compared to those fed the SU diet, besides reducing lipid synthesis from glucose in hepatic tissue. Thus, the inclusion of n-3 LCPUFAs in the diet may be beneficial for the prevention or attenuation of dyslipidemia and insulin resistance, and for reducing the risk of related chronic diseases.

Effects of hypo- or hyperosmotic stress on lipid synthesis and gluconeogenic activity in tissues of the crab Neohelice granulata.

The present study assesses the effects of osmotic stress on phosphoenolpyruvate carboxykinase (PEPCK), fructose 1,6-bisphosphatase (FBPase) and glucose 6-phosphatase (G6Pase) activities and (14)C-total lipid synthesis from (14)C-glycine in the anterior and posterior gills, jaw muscle, and hepatopancreas of Neohelice granulata. In posterior gills, 24-h exposure to hyperosmotic stress increased PEPCK, FBPase and G6Pase activities. Increase in (14)C-lipid synthesis was associated to the decrease in PEPCK activity after 72-h exposure to hyperosmotic stress. Hypo-osmotic stress decreased PEPCK and G6Pase activities in posterior gills; however, (14)C-lipids increased after 72-h exposure to stress. In anterior gills, decreases in the G6Pase activity after 72-h of hyperosmotic stress and in (14)C-lipogenesis after 144-h were observed, while PEPCK activity increased after 144 h. Exposure to hypo-osmotic stress increased (14)C-lipid synthesis and PEPCK activity in anterior gills. Muscle G6Pase activity increased after 72-h exposure to hypo-osmotic stress; however, no significant change was observed in the lipogenesis. PEPCK decreased in muscle after 144-h exposure to hyperosmotic, coinciding with increased (14)C-lipid synthesis. In the hepatopancreas, a decrease in the (14)C-lipogenesis occurred after 24-h exposure to hyperosmotic stress, accompanied by increase in (14)C-lipid synthesis. Additionally, PEPCK activity returned to control levels. The hepatopancreatic lipogenesis from amino acids was not involved in the metabolic adjustment during hypo-osmotic stress. However, gluconeogenesis is one of the pathways involved in the adjustment of the intracellular concentration of nitrogenated compounds.

Serum S100B protein is increased in fasting rats.

BACKGROUND: S100B is a calcium-binding protein expressed and secreted by astrocytes; serum and cerebrospinal fluid (CSF) S100B elevation has been proposed as an index of brain damage. However, other tissues are shown to produce this protein and the clinical significance of serum S100B elevation has been discussed. METHODS: We investigated the levels of serum and CSF S100B in fasting Wistar rats. Animals were divided into two groups, control and fasting for 48 h, and S100B levels in serum and CSF were determined by ELISA. S100B secretion in dissociated epididymal fat cells was investigated in the presence of epinephrine. RESULTS: We observed a significant >2-fold increase of S100B levels in serum of fasting rats, without changes in its CSF content. Moreover, we demonstrated in vitro epinephrine stimulated S100B release from fat cells. CONCLUSIONS: Present results reinforce that extracerebral sources of S100B, particularly adipocytes, contribute to its serum levels and support the idea that caution is needed when interpreting serum S100B increase as a clinical marker of brain damage.