ABSTRACT:Researchers and physicians look forward to effective therapeutic agents possibly from medicinal plants following the ineffectiveness of modern drugs used in the treatment of fatty liver and its related diseases. To this ends, we evaluated the effect of Cyperus esculentus on the liver in experimentally induced hyperlipidemia in rats.Aqueous extract of the plant was administered orally to rats at the doses of 300,400 and 600mg/kg body weight(b.wt) for a period of twenty nine days. Fatty liver was induced by twice intraperitoneal injection of TritonWR-1339 at a dose of 300mg/kg b.wt. to wistar rats . The result shows that administration of triton led to significant (P˂0.05) serum increase in the activities of alanine and aspartate aminotransferases (ALT and AST) of the rats.There was no significant (p˃0.05) change in the activities of serum alkaline phosphatase following the administration of triton.The study also shows that there were significant( p˂0.05) reduction in the serum level of total protein , albumin and globulin and increase in serum level of total and conjugated bilirubin though not statistically significant (p˃0.05) following the administration of triton to rats.The observed effects are suggestive of mild toxicity of the liver by triton and this is further supported by several histopathological manifestations such as hepatocellular degeneration, macrovesicular vacuolation,periportal necrosis, congestion ,severe intimal ulceration and stenosis in the blood vessels . Treatment with the aqueous extract of Cyperus esculentus attenuated both the biochemical effects and histopathological manifestations.In conclusion, the results from the serum liver enzymes biochemical parameters and histopathological analyses suggested the toxicity of triton and also showed the effectiveness of the aqueous extract of Cyperus esculentus in attenuating the liver toxicity .©JASEM https://dx.doi.org/10.4314/jasem.v21i4.7

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The present study was carried out to evaluate the Acute toxicity, hepatoprotective and in-vivo antioxidant activities of ethanolic extract of Caesalpinia bonduc leaf on carbon tetrachloride (CCl4) induced liver damage using Swiss albino rats . The ethanolic extract of the plant of C. bonduc were suspended in 5 % tragacanth and then administered orally at doses of 250 and 500 mg/kg body weight for fourteen days before intraperitoneally injection of Carbon tetrachloride (CCl4) at dose of 2 mL/kg body weight. The plant extracts at 250 and 500mg/kg b.wt showed a remarkable hepatoprotective and invivo antioxidant activities against carbon tetrachloride CCl4 – induced hepatotoxity judged from the serum marker enzymes .The CCl4 induced significant increase in aspartate amino transferase( AST), alanine amino transferase (ALT), alkaline phophatase (ALP), total bilirubin, and malondyaldehyde (MDA) with a reduction of total protein, catalase, and glutathione peroxidase . Treatment of rats with different doses of plant extract (250 and 500 mg/kg b.wt.) significantly (P< 0.001) altered serum maker enzymes and antioxidant levels to near normal levels. The study suggests that C. Bonduc specifically chloroform and ethyl acetate fraction may be good sources of natural antioxidant and hepatoprotective substance.Keywords: Ceasalpiniabonduc, hepatoprotective, intraperitoneally , antioxidant

Insulin is an anabolic hormone that plays key roles in glucose metabolism. Insulin resistance is a decreased biological response to normal concentration of circulating insulin. In insulin resistance, normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells. Insulin resistance in fat cells results in hydrolysis of stored triglycerides, which elevates free fatty acids in the blood plasma. In muscles, it reduces glucose uptake, whereas in the liver, it reduces glucose storage with both effects serving to elevate blood glucose. High plasma levels of Insulin and glucose due to Insulin resistance often lead to metabolic syndrome and type 2 diabetes mellitus. The cause of the vast majority of cases of insulin resistance remains unknown. However, it is claimed that insulin resistance might be caused by a high carbohydrate diet. Studies have shown that glucosamine (often prescribed for joint problems) may cause Insulin resistance. It is also reported that insulin resistance occurrence in a population increased as sugar consumption and addition of high fructose corn syrup to diets increased. Physical inactivity and obesity have been implicated as factors, which aggravate insulin resistance. The presumption that a defect in specific gene may cause insulin resistance is still under investigation.