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.

Pulmonary hypertensive response of broiler chickens to arginine and guanidinoacetic acid under high-altitude hypoxia.

This study assessed the preventive effects of arginine (ARG) and guanidinoacetic acid (GAA) on the incidence of pulmonary hypertension syndrome (PHS) in broiler chickens. Four isoenergetic and isonitrogenous diets were prepared, including: (i) the control, (ii) the control supplemented with 1 g/kg ARG, (iii) the control supplemented with 1 g/kg GAA, and (iv) the control supplemented with 1.5 g/kg GAA. These diets were fed to broilers (Ross 308) from day 1 to 42 post-hatch. Criteria evaluated in the experiment were growth performance, carcass characteristics, serum and blood variables, lead-II electrocardiogram, and ET-1 and iNOS gene expression in heart and lungs. Mortality from PHS was recorded daily. The results showed that ARG and GAA supplements improved the feed conversion ratio (FCR) compared to the control (P < 0.05). Supplementation of ARG and GAA significantly (P < 0.05) increased serum nitric oxide (NO) concentration. ARG and GAA supplementation significantly reduced the haematocrit value and the heterophil to lymphocyte ratio in the blood. A significant (P < 0.05) decline in S-wave amplitude of the lead-II electrocardiogram, right to total ventricular weight ratio (RV:TV) and ascites mortality was observed by supplementing ARG or 1.5 g/kg GAA. Addition of ARG and GAA supplements did not significantly change ET-1 and iNOS gene expression in the heart and lung relative to the control. In conclusion, GAA supplementation at 1.5 g/kg had a potential to improve growth performance and could prevent PHS.