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

Author:
Quines, Caroline B., Rosa, Suzan G., Chagas, Pietro M., Velasquez, Daniela, Prado, Vinicius C., Nogueira, Cristina W.
Source:
Food and chemical toxicology 2017
ISSN:
0278-6915
Subject:
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
Abstract:
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.