Effects of Pioglitazone, Glimepiride, Nobivolol, Valsartan and Hesperidine on Serum Diabetic Marker and Lipid Metabolizing Enzymes in Isoproterenol Induced Myocardial Infarction in Normal and Diabetic Rats

Abstract

Present study was designed to evaluate effect some synthetic drugs and some herbal compound on Glucose, HbA1c and Lipid Metabolizing Enzymes in isoproterenol induced myocardial infarction in normal and Streptozoto-cin-Nicotinamide induced diabetic in rats. Pioglitazone (10 mg/kg, p.o), Glimepiride (0.5 mg/kg, p.o), Nobivolol (2 mg/kg, p.o), Valsartan (8 mg/kg, p.o) and Hesperidin (100 mg/kg, p.o) were administered for 28 days in rats in-jected with single dose of Streptozotocin (65 mg/kg, i.p, STZ) and Nicotinamide (12mg/kg, i.p, NIC) and after iso-proterenol (200 mg/kg, s.c.) induced myocardial infarction in rats on 29th and 30th day. At the end of experimen-tal period (i.e. on the day 31) serum and heart tissues sample were collected, and glucose, HbA1c and cholesterol ester synthetase (CES), lecithin Cholesterol acyl transferase (LCAT), lipoprotein lipase (LPL) were find out. Adminis-tration of STZ–NIC in rats showed a significant (p<0.001) increased in the levels of serum glucose, glycosylated hemoglobin (HbA1c), significant (p<0.001) increased in the level of heart tissues CES and significant (p<0.001, p<0.01) decreased LCAT and LPL as compared to respective control groups. Treatment with Pioglitazone, Glimepi-ride significantly (P<0.001) decreased and Hesperidin significant (P<0.05) decreased HbA1c, glucose and CES level but treatment with nobivolol significant (p<0.05) decreased CES level without change on glucose and HbA1c. Treatment with Pioglitazone and Glimepiride significantly (P<0.001) increased and Hesperidin and Nobivolol (P<0.01) increased LCAT and LPL as compared to diabetic control. Treatment with Valsartan shows no change on Glucose, HbA1c and lipid metabolizing enzyme in diabetic rats. This study concluded that Pioglitazone and Glime-piride may show reduced diabetes marker, CES and protect LCAT and LPL on experimentally induced myocardial infarction in type 2 diabetic rats.