ABSTRACT
Sitagliptin is highly selective dipeptidyl peptidase-4 [DPP-4] inhibitor that is considered as one of the new oral therapies for management of type II diabetes. Because of the sitagliptin unknown effects on the endocrine part of the pancreas, especially on the cellular levels, this study was done to evaluate its effect on the endocrine part of the pancreas in experimentally-induced type II diabetic in adult albino rats. The present study was carried out on 30 adult male albino rats which were divided into; Group I [untreated control group], Group II [diabetic group], where type II diabetes had been induced via alloxan intake] and group III [treated group], where 0.14 mg/100 mg B.W. sitagliptin was given orally per day for 3 weeks after induction of type-2 diabetes. The specimens were prepared for light microscopic examination. In parallel, the related biomedical parameters such as serum glucose and serum insulin levels had been estimated, statistically analyzed and compared between the three groups. Sections of pancreas taken from diabetic rats showed morphological changes in islets of Langerhans cells in the form of pyknotic nuclei, cytoplasmic vacuolation, poor differentiation and abnormal shape and size of the cells. These morphological changes had been partially recovered in diabetic rats treated with sitagliptin. Also, the hyperglycemia and hypoinsulinemia that was detected in the control diabetic group had been nearly returned to normal after sitagliptin treatment. Sitagliptin drug has improved islet functions on both morphological and biomedical parameters in type II diabetic rats and can be taken into consideration as one of the new oral anti- diabetic drugs on the human level that need to be more investigated
Subject(s)
Animals, Laboratory , Triazoles/adverse effects , Pancreas/pathology , Histology , Diabetes Mellitus, Experimental/complications , RatsABSTRACT
Acetaminophen, a widely used analgesic and antipyretic is known to cause hepatic injury in humans and experimental animals when administered in high doses. It was reported that toxic effects of acetaminophen are due to oxidative reactions that take place during its metabolism. L-carnitine is a cofactor in the transfer of long-chain fatty acid allowing to the beta-oxidation of fatty acid in the mitochondria. It is a known antioxidant with protective effects against lipid peroxidation. This study aimed to investigate the possible beneficial effect of L-carnitine as an antioxidant agent against acetaminophen induced hepatic toxicity in rats. Four rat groups [N=7 in each group]. Group I is the control, group II received 500 mg/kg/ body weight of L-carnitine for 7 days by oral route, group III received 640/kg/ bw of acetaminophen by oral route, group IV acute acetaminophen group pretreated with L-carnitine for 7 days by gastric tube gavage tube. The liver of all rats were removed for investigation using light and electro microscopic studies. Acetaminophen caused massive centrilobular necrosis and massive degenerative changes. The electron-microscopic study showed few mitochondria, increased fat droplets and scanty smooth endoplasmic reticulum [SER], rough endoplasmic reticulum [RER].These changes were reduced by L-carnitine pretreatment. Those results suggest that acetaminophen results damage in the liver as an acute effect and L-carnitine ameliorated the adverse effects of acetaminophen via its antioxidant role