Effect of coconut oil on lipid profile and antioxident status in rats

Abstract

The study was conducted to evaluate the effect of various preparations of coconut oil (copra oil, seasoned coconut oil and virgin coconut oil) and fish oil on lipid profile and antioxidant status in rats. Adult male Wistar rats (180-220 g) were randomly divided into five groups and administered with oils as follows: G1 – normal control (NC), G2 – copra oil (CO), G3 – seasoned coconut oil (SCO), G4 - virgin coconut oil (VCO) and G5 – fish oil (FO). Oils were administered orally to rats at a dose of 16.4g/kg body weight per day using an orogastric tube for a period of 90 days. Blood samples were collected on day 0 (before oil administration), 45 and 90 and serum was separated. Body weight was also recorded on the above days. Animals were euthanized on day 90; liver and heart were separated and weighed. Serum were analyzed for biochemical parameters viz., TAG, TL, TC, HDL, LDL and VLDL and tissues for TC, TAG, LP and GSH. Liver glycogen was also estimated. Representative samples of liver and heart tissues were subjected to histopathological examination. Administration of CO and SCO for 3 months did not show any significant variation in body weight. VCO administration significantly (P< 0.05) decreased whereas, FO administration significantly (P< 0.05) increased the body weight, when compared to NC. Serum TAG and VLDL were significantly (P< 0.05) increased while, LDL was decreased by CO administration. Serum TL, TC and HDL were similar to that of NC. SCO administered rats showed significantly (P< 0.05) higher levels of TL, TC, TAG, HDL, LDL and VLDL. VCO administration significantly (P< 0.05) increased the level of HDL and decreased LDL. Moreover, VCO administered rats did not show any significant variation in the levels of TL, TAG, TC and VLDL. Administration of FO showed the levels of TC, HDL and VLDL similar to that of NC, but TAG increased significantly (P< 0.05) and TL and LDL showed a significant (P< 0.05) reduction. When HDL/LDL ratio was compared, CO, VCO and FO administered rats showed higher values when compared to NC. SCO administered rats, showed a value similar to that of day 0 but VCO administered group showed the highest value. Administration of CO and FO significantly (P< 0.05) increased the weight of liver and heart while VCO administration did not show any significant variation from that of NC. SCO significantly (P< 0.05) decreased weight of liver whereas, weight of heart was similar to that of NC. Level of liver glycogen decreased significantly (P< 0.05) in all oil administered groups except VCO, which showed a level similar to that of NC. Administration of CO significantly (P< 0.05) increased the level of TC in heart and TAG in both the tissues, while TC in liver was similar to that of NC. SCO administration significantly (P< 0.05) increased TC whereas, the TAG levels were similar to that of NC in both the tissues. VCO consumption significantly (P< 0.05) decreased the level of TC in both the tissues, while it increased TAG in heart without affecting liver TAG. FO administration did not show any significant variation in the level of TC and TAG in heart, but it significantly (P< 0.05) decreased the level of TC without affecting liver TAG. Administration of CO and FO significantly (P< 0.05) increased the levels of LP and GSH in both the tissues except for liver GSH in FO group, which was similar to that of NC. Feeding SCO maintained the level of LP in both the tissues, while GSH increased significantly (P< 0.05) in heart while its level in liver was unaffected. VCO intake significantly (P< 0.05) reduced the level of both LP and GSH in heart, but maintained the normal level in liver. Hepatocytes of rats administered with CO showed diffused necrosis with vacuolation and central venous congestion and lesions in heart were characterized by congestion and moderate hyalinization. SCO administered rats showed dilatation of sinusoids and diffuse congestion of liver but histological architecture in heart tissue was normal. VCO and FO administration exhibited normal histological architecture of both liver and heart except for a mild degeneration of hepatocytes in VCO consumed group. Based on the above observations it could be suggested that long term consumption of VCO and FO might not cause any adverse effects on serum and tissue lipid profile except for oxidative stress by FO. CO and SCO feeding revealed some adverse effects, but it is worth mentioning that the dose of oil administered (16.4 g/kg body weight, i.e. 30 kg/head/year) was very high, which stands in between per capita world average consumption (17.8 kg/head/year) and consumption of developed western world (44 to 48 kg/head/year), also which is more than double the per capita coconut oil consumption in Kerala (14 kg/head/year). Therefore, consumption of CO and SCO at a lower dose or the per capita consumption in Kerala as stated above might not elicit adverse effects as observed in the present study.