Innovative insights into the effects of a high-sucrose diet on pancreatic health and the therapeutic role of empagliflozin in type 2 diabetes: An experimental study.

Type 2 Diabetes (T2D) is a growing global health issue, often aggravated by excessive sugar intake. Chronic high-sucrose diets contribute to insulin resistance, oxidative stress, and pancreatic dysfunction, worsening metabolic health. Sodium-glucose co-transporter 2 (SGLT2) inhibitors, like empagliflozin, show potential in improving glycemic control and metabolic parameters, but their effects on pancreatic efficiency in sugar-induced T2D are not well understood. This study aimed to explore the effects of empagliflozin on metabolic and pancreatic protection in a high-sucrose diet-induced T2D model. Male Wistar rats were divided into four groups: normal, normal-treated, diabetic, and diabetic-treated (n = 8 per group). Diabetes was induced with a 35% sucrose solution for 8 weeks, followed by a low-dose streptozotocin (STZ) injection. Treated groups received empagliflozin (15 mg/kg/day) for the duration. Biochemical markers, including fasting blood sugar (FBS), lipid profile, insulin levels, and oxidative stress markers, were measured. Insulin resistance (HOMA-IR) and pancreatic function (HOMA-B) were assessed. Histological analysis of pancreatic tissues was performed. The high-sucrose diet increased FBS, insulin resistance, and oxidative stress, while decreasing pancreatic function and islet diameter. Empagliflozin treatment lowered FBS (p = 0.001), improved insulin sensitivity (p = 0.001), reduced triglycerides (p = 0.001), and LDL (p = 0.05). It also enhanced antioxidant enzymes, reduced lipid peroxidation (MDA, p = 0.001), and preserved pancreatic islet structure (p = 0.001). A high-sucrose diet negatively affects metabolic health and pancreatic function. Empagliflozin mitigates these effects by improving metabolism, reducing oxidative stress, and preserving pancreatic integrity, suggesting its potential as a therapeutic agent in diabetes related to excessive sugar consumption.