Effect of magnesium sulfate administration to improve insulin resistance in type 2 diabetes animal model: using the hyperinsulinemic-euglycemic clamp technique.

This study attempted to elucidate the possible mechanism of magnesium sulfate (MgSO4 ) administration on reducing insulin resistance in type 2 diabetic rats. Fifty Wistar rats were divided into five groups: NDC was fed the normal diet, CD received high-fat diet with 35 mg/kg of streptozotocin, CD-Mg animals received MgSO4 via drinking water, CD-Ins1, and CD-Ins2 animals treated with low or high dose of insulin. Body weight and blood glucose levels were measured weekly. Intraperitoneal glucose tolerance test (IPGTT), insulin tolerance test, and metabolic cage assessment were performed monthly. After 12 weeks, the hyperinsulinemic-euglycemic clamp was performed for all animals and blood sample was taken to measure glycated hemoglobin (HbA1c), plasma insulin, glucagon, calcium, and magnesium levels. Liver and gastrocnemius muscle were isolated to measure glucagon receptor (GR), Glucose 6 phosphatase (G6Pase), Phosphoenolpyruvate carboxykinase (Pepck) and Glucose transporter 4 (Glut4) genes expression and GLUT4 protein translocation into the cell membrane. Consuming of high-fat diet generated insulin-resistant rats. Magnesium or insulin therapy altered insulin resistance, blood glucose, IPGTT, gluconeogenesis pathway, GR, body weight, the percentage of body fat, and HbA1C in diabetic rats. Administrations of MgSO4 or insulin in Type 2 diabetes mellitus animals increase GLUT4 gene and protein expression. Mg could improve glucose tolerance via stimulation of Glut4 gene expression and translocation and also suppression of the gluconeogenesis pathway and GR gene expression. Mg also increased glucose infusion rate and displayed beneficial effects in the treatment of glucose metabolism and improved insulin resistance.

Stress biomarker responses to different protocols of forced exercise in chronically stressed rats.

Stress is one of the most significant causes of major health problems on a global scale. The beneficial effects of exercise on combating stress, however, are well-established. The present study investigated the stress biomarker responses, such as serum corticosterone, interlukin-1ß, and glucose levels, to different (preventive, therapeutic, protective, and continuous) protocols of forced exercise under stress. Male rats were randomly allocated to the following five groups: stressed, preventive, therapeutic, protective, and continuous (and/or pre-stress, post-stress, stress-accompanied, and both pre-stress and stress-accompanied exercise respectively) exercise groups. Stress was applied 6 h/day for 21 days and the treadmill running was employed at a speed of 20-21 m/min for 21 and 42 days. The findings showed that the therapeutic, protective, and continuous exercises led to reduced corticosterone and glucose levels. Whereas, the preventive exercise did not reverse the stress responses, and that the therapeutic exercise led to a significant decline in serum interlukin-1ß. It is concluded that protective, therapeutic, and, particularly, continuous exercises lead to significant reductions in serum corticosterone and the associated stress-induced hyperglycemia. Moreover, it appears that the timing and duration of exercise are the two factors contributing to changes in stress biomarker responses.

Preventive and therapeutic effect of treadmill running on chronic stress-induced memory deficit in rats.

Previous results indicated that stress impairs learning and memory. In this research, the effects of preventive, therapeutic and regular continually running activity on chronic stress-induced memory deficit in rats were investigated. 70 male rats were randomly divided into seven groups as follows: Control, Sham, Stress-Rest, Rest-Stress, Stress-Exercise, Exercise-Stress and Exercise-Stress & Exercise groups. Chronic restraint stress was applied 6 h/day for 21days and treadmill running 1 h/day. Memory function was evaluated by the passive avoidance test. The results revealed that running activities had therapeutic effect on mid and long-term memory deficit and preventive effects on short and mid-term memory deficit in stressed rats. Regular continually running activity improved mid and long-term memory compared to Exercise-Stress group. The beneficial effects of exercise were time-dependent in stress conditions. Finally, data corresponded to the possibility that treadmill running had a more important role on treatment rather than on prevention on memory impairment induced by stress.