Asian Journal of Research and Reports in Endocrinology

The pancreas is a glandular organ endowed with two main functions; an exocrine function that assists digestion and an endocrine function that modulates blood glucose concentration. Pancreatic Beta-cells produce insulin to regulate/lower blood glucose concentration, driving them into cells to be utilized. Distortions of the architecture of pancreatic Beta-cells lead to function loss; thus, preservation/restoration of their cyto-architecture would sustain their functions. Vernonia amygdalina is a vital plant acknowledged widely for its antioxidant and anti-diabetic effects; however, its impact on the pancreas has received little attention. This study is premeditated to examine the effects of the methanolic leaf extracts of Vernonia amygdalina (MLEVA) on the cyto-architecture of the pancreas in Alloxan-induced pancreatic toxicity. Thirty (30) adult male Wistar rats were grouped into 6 (A-F) (n=5). Group A, the control group, received feed and water only. Group B received a single intra-peritoneal injection of 150mg/kg of Alloxan. Groups C, D, and E received single intra-peritoneal injections of 150mg/kg of Alloxan and were then treated with 200, 300, and 400 mg/kg/day of the MLEVA, respectively. Group F received a single intra-peritoneal injection of 150mg/kg of Alloxan and was orally treated with 100mg/kg/day of Vitamin E. The experiment lasted 16 days before sacrificing the animals via a median incision on the abdominal cavity, under ketamine (100mg/ml), as anaesthesia, 24 hours after their last treatment. The pancreas was carefully and rapidly processed for routine H & E staining. This study recorded a 28% mortality rate after Alloxan administration, leading to degenerative histo-pathological changes in the pancreas' endocrine and exocrine compartments. 300mg/kg of MLEVA demonstrated a marked regenerative effect on the pancreas. The MLEVA is a promising agent for managing Diabetes, evidenced by its protective and therapeutic effect on Alloxan-induced pancreatic toxicity.