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(p-ClPhSe)2 stimulates carbohydrate metabolism and reverses the metabolic alterations induced by high fructose load in rats

Quines, Caroline B., Rosa, Suzan G., Chagas, Pietro M., Velasquez, Daniela, Prado, Vinicius C., Nogueira, Cristina W.
Food and chemical toxicology 2017
adenosine triphosphate, blood glucose, carbohydrate metabolism, citrate (si)-synthase, dose response, fructose, glucose, glycogen, hexokinase, homeostasis, humans, isocitrate dehydrogenase, lipid metabolism, liver, rats, skeletal muscle, toxicology, triacylglycerols, tricarboxylic acid cycle
The modern life leads to excess consumption of food rich in fructose; however, the long-term changes in carbohydrate and lipid metabolism could lead to metabolic dysfunction in humans. The present study evaluated the in vitro insulin-mimetic action of p-chloro-diphenyl diselenide (p-ClPhSe)2. The second aim of this study was to investigate if (p-ClPhSe)2 reverses metabolic dysfunction induced by fructose load in Wistar rats. The insulin-mimetic action of (p-ClPhSe)2 at concentrations of 50 and 100 μM was determined in slices of rat skeletal muscle. (p-ClPhSe)2 at a concentration of 50 μM stimulated the glucose uptake by 40% in skeletal muscle. A dose-response curve revealed that (p-ClPhSe)2 at a dose of 25 mg/kg reduced (∼20%) glycemia in rats treated with fructose (5 g/kg, i.g.). The administration of fructose impaired the liver homeostasis and (p-ClPhSe)2 (25 mg/kg) protected against the increase (∼25%) in the G-6-Pase and isocitrate dehydrogenase activities and reduced the triglyceride content (∼25%) in the liver. (p-ClPhSe)2 regulated the liver homeostasis by stimulating hexokinase activity (∼27%), regulating the TCA cycle activity (increased the ATP and citrate synthase activity (∼15%)) and increasing the glycogen levels (∼67%). In conclusion, (p-ClPhSe)2 stimulated carbohydrate metabolism and reversed metabolic dysfunction in rats fed with fructose.