Quines Caroline B, Rosa Suzan G, Chagas Pietro M, Velasquez Daniela, Prado Vinicius C, Nogueira Cristina W
Laboratório de Síntese, Reatividade e Avaliação Farmacológica e Toxicológica de Organocalcogênios, Centro de Ciências Naturais e Exatas, Departamento de Bioquímica e Biologia Molecular, Universidade Federal de Santa Maria, Santa Maria CEP 97105-900, RS, Brazil.
Laboratório de Síntese, Reatividade e Avaliação Farmacológica e Toxicológica de Organocalcogênios, Centro de Ciências Naturais e Exatas, Departamento de Bioquímica e Biologia Molecular, Universidade Federal de Santa Maria, Santa Maria CEP 97105-900, RS, Brazil.
Food Chem Toxicol. 2017 Sep;107(Pt A):122-128. doi: 10.1016/j.fct.2017.06.038. Epub 2017 Jun 24.
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). The second aim of this study was to investigate if (p-ClPhSe) reverses metabolic dysfunction induced by fructose load in Wistar rats. The insulin-mimetic action of (p-ClPhSe) at concentrations of 50 and 100 μM was determined in slices of rat skeletal muscle. (p-ClPhSe) at a concentration of 50 μM stimulated the glucose uptake by 40% in skeletal muscle. A dose-response curve revealed that (p-ClPhSe) 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) (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) 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) stimulated carbohydrate metabolism and reversed metabolic dysfunction in rats fed with fructose.
现代生活导致富含果糖的食物摄入过量;然而,碳水化合物和脂质代谢的长期变化可能会导致人类代谢功能障碍。本研究评估了对氯二苯基二硒醚(p-ClPhSe)的体外胰岛素模拟作用。本研究的第二个目的是调查(p-ClPhSe)是否能逆转Wistar大鼠果糖负荷诱导的代谢功能障碍。在大鼠骨骼肌切片中测定了浓度为50和100μM的(p-ClPhSe)的胰岛素模拟作用。浓度为50μM的(p-ClPhSe)可使骨骼肌中的葡萄糖摄取增加40%。剂量反应曲线显示,剂量为25mg/kg的(p-ClPhSe)可使接受果糖(5g/kg,腹腔注射)治疗的大鼠的血糖降低(约20%)。果糖给药损害了肝脏内环境稳态,而(p-ClPhSe)(25mg/kg)可防止葡萄糖-6-磷酸酶和异柠檬酸脱氢酶活性增加(约25%),并降低肝脏中的甘油三酯含量(约25%)。(p-ClPhSe)通过刺激己糖激酶活性(约27%)、调节三羧酸循环活性(增加ATP和柠檬酸合酶活性(约15%))以及增加糖原水平(约67%)来调节肝脏内环境稳态。总之,(p-ClPhSe)刺激了碳水化合物代谢,并逆转了喂食果糖的大鼠的代谢功能障碍。