Syzygium samarangense fruit extract attenuates hyperglycemia in type 2 diabetic rats through modulation of oxidative...

The global incidence of type 2 diabetes mellitus (T2DM), a chronic metabolic disorder, is on the rise, with persistent hyperglycemia contributing to vascular complications. The present study aimed to assess the preventive effects of Syzygium samarangense fruit extract (SSE) on pancreatic β cell dysfunction and associated metabolic disturbances in a diabetic rat model. Male Wistar rats were rendered diabetic through a high-fat diet combined with a low dose of streptozotocin and subsequently divided into four groups: Normal control, diabetic control, diabetic treated with SSE (400 mg/kg) and diabetic treated with glibenclamide (5 mg/kg), a sulfonylurea insulin secretagogue used as a positive control. Treatments were administered orally for 4 weeks. Biochemical assessments included evaluation of fasting blood glucose, insulin concentrations in both serum and pancreatic tissue, oxidative stress indicators such as malondialdehyde (MDA), activities of key antioxidant enzymes including catalase (CAT) and superoxide dismutase (SOD) and levels of the pro-inflammatory cytokine TNF-α, the hepatic gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK) and liver function enzymes. Administration of SSE resulted in a moderate decrease in blood glucose and a significant increase in insulin levels in both serum and pancreatic tissue. SSE enhanced the activities of antioxidant enzymes CAT and SOD, while significantly decreasing MDA levels, indicating mitigated oxidative stress. A notable decrease in TNF-α was also observed, supporting the anti-inflammatory potential. Furthermore, suppression of PEPCK expression and improved liver enzyme profiles were noted, demonstrating inhibition of hepatic gluconeogenesis and hepatoprotection. Collectively, the present study demonstrates that SSE contributes to improved glucose homeostasis in diabetic rats, primarily by mitigating oxidative stress, inflammation and hepatic dysfunction. These findings support its potential application as a complementary therapy in T2DM.