Effects of Honey on Postprandial Hyperlipidemia and Oxidative Stress in Wistar Rats: Role of HMG-CoA Reductase Inhibition and Antioxidant Effect.

Postprandial hyperlipidemia is associated with oxidative stress and is an important risk factor for atherosclerosisand cardiovascular disease. The aims of this study were to investigate the antihyperlipidemic effect of honey administered 5or 60 minutes before a high-fat diet (HFD), to explore the role of 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA)reductase in antihyperlipidemic effect of honey and to investigate the effect of honey on postprandial oxidative stress. Ratswere fasted and randomized into 5 groups. Groups 1 and 2 were administered portable water. After 60 minutes, the groupswere given portable water and HFD, respectively. Group 3 was administered honey. After 5 minutes, the rats were givenHFD. Groups 4 and 5 were administered honey and simvastatin, respectively. After 60 minutes, the rats were given HFD.Four hours after portable water or HFD administration, the rats were sacrificed. Group 2 had significantly (p < 0.01) highertotal cholesterol (TC), triglycerides (TG), low density lipoprotein (LDL) cholesterol, very low density lipoprotein (VLDL)cholesterol, catalase activity and significantly (p < 0.05) lower high density lipoprotein (HDL) cholesterol and HMG-CoA:mevalonate (p < 0.001) compared with Group 1. Group 3 had significantly (p < 0.01) higher TG and VLDL cholesterol andlower HMG-CoA: mevalonate compared with Group 1. Groups 4 and 5 exhibited significantly (p < 0.05 or p < 0.001) higherHDL cholesterol and HMG-CoA: mevalonate and lower LDL cholesterol compared with group 2. Honey pretreatment 60minutes before HFD feeding exerts more significant antihyperlipidemic effect and attenuates more considerably postprandialhyperlipidemia-induced oxidative stress than honey administered 5 minutes before HFD in Wistar rats. This markedantihyperlipidemic effect of honey pretreatment is mediated in part via inhibition of HMG-CoA reductase.

Hypoglycemic and antioxidant effects of honey supplementation in streptozotocin-induced diabetic rats.

OBJECTIVES: Oxidative stress plays a crucial role in the development of diabetic complications. The aims of this study were to investigate whether honey could reduce hyperglycemia and ameliorate oxidative stress in kidneys of streptozotocin-induced diabetic rats. METHODS: Diabetes was induced by a single dose of STZ (60 mg/kg; i. p.). Diabetic rats were randomly grouped and administered distilled water (0.5 mL/day) and honey (0.2 g/kg/day, 1.2 g/kg/day and 2.4 g/kg/day) by oral gavage for four weeks. Each group consisted of six rats. RESULTS: Total antioxidant status (TAS), activities of catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione-S-transferase (GST) were significantly reduced, while superoxide dismutase (SOD) activity was up-regulated in kidneys of diabetic rats. Lipid peroxidation (TBARS) and fasting plasma glucose (FPG) were significantly elevated while body weight was reduced in diabetic rats. Honey significantly increased body weight, TAS, activities of CAT, GPx, GR, and GST in diabetic rats. It significantly restored SOD activity, and reduced FPG and TBARS levels in diabetic rats. Histopathological examinations of the kidneys revealed that mesangial matrix expansion and thickening of glomerular basement membrane were reduced in the honey-treated diabetic rats. CONCLUSIONS: Honey exerts a hypoglycemic effect and ameliorates oxidative stress in kidneys of streptozotocin-induced diabetic rats.

Antioxidant protection of Malaysian tualang honey in pancreas of normal and streptozotocin-induced diabetic rats.

Glucotoxicity contributes to beta-cell dysfunction through oxidative stress. Our previous study demonstrated that tualang honey ameliorated renal oxidative stress and produced hypoglycemic effect in streptozotocin (STZ)-induced diabetic rats. This present study investigated the hypothesis that hypoglycemic effect of tualang honey might partly be due to protection of pancreas against oxidative stress. Diabetes was induced by a single dose of STZ (60 mg/kg; ip). Diabetic rats were randomly divided into two groups and administered distilled water (0.5 ml/d) and tualang honey (1.0 g/kg/d). Similarly, two groups of non-diabetic rats received distilled water (0.5 ml/d) and tualang honey (1.0 g/kg/d). The animals were treated orally for 28 days. At the end of the treatment period, the honey-treated diabetic rats had significantly (p<0.05) reduced blood glucose levels [8.8 (5.8)mmol/L; median (interquartile range)] compared with the diabetic control rats [17.9 (2.6)mmol/L]. The pancreas of diabetic control rats showed significantly increased levels of malondialdehyde (MDA) and up-regulation of superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. Catalase (CAT) activity was significantly reduced while glutathione-S-transferase (GST) and glutathione reductase (GR) activities remained unchanged in the pancreas of diabetic rats. Tualang honey significantly (p<0.05) reduced elevated MDA levels. Honey treatment also restored SOD and CAT activities. These results suggest that hypoglycemic effect of tualang honey might be attributed to its antioxidative effect on the pancreas.