Objective: This study aimed to investigate the effects of Perga supplementation on glucose metabolism, body weight regulation, and amyloid-beta (Aβ) accumulation in a streptozotocin (STZ)-induced type 2 diabetes (T2D) rat model, focusing specifically on insulin, leptin, and fibroblast growth factor 21 (FGF21) signaling pathways.
Methods: Male Wistar rats were divided into Sham (S), T2D, and T2D+Perga (T2DP) groups. T2D was induced by a single intraperitoneal (i.p.) STZ injection (60 mg/kg). Perga (200 mg/kg/day) was administered to the T2DP group by gavage 14 days after diabetes induction. Plasma and brain insulin and leptin levels, liver and plasma FGF21 concentrations, Homeostasis Model Assessment of Beta Cell Function (HOMA-β) index, fasting glucose levels, body weight changes, and brain amyloid-beta (Aβ) accumulation were evaluated.
Results: STZ-induced T2D resulted in hypoinsulinemia, decreased HOMA-β scores, weight loss, reduced plasma leptin, increased brain leptin, decreased FGF21 levels, and significant Aβ accumulation in the hippocampus. Perga treatment significantly improved plasma and brain insulin levels, increased HOMA-β, reduced fasting glucose, and attenuated weight loss. Plasma leptin levels returned to normal, brain leptin levels decreased, and hippocampus Aβ burden was significantly reduced. In addition, perga supplementation almost normalized liver and plasma FGF21 levels.
Conclusion: Perga supplementation effectively ameliorates metabolic dysfunction and neurodegenerative markers in the T2D model. Its regulatory effects on insulin, leptin, and FGF21 signaling highlight its potential as a natural therapeutic agent in managing T2D and associated AD-like pathology. Further research is needed to evaluate its clinical applicability.
Akdeniz University Animal Research Ethics Local Committee (Ethics Approval Number: 2025.04.B.001)
| Primary Language | English |
|---|---|
| Subjects | Veterinary Sciences (Other) |
| Journal Section | Research Article |
| Authors | |
| Submission Date | May 21, 2025 |
| Acceptance Date | December 11, 2025 |
| Publication Date | December 31, 2025 |
| Published in Issue | Year 2025 Volume: 44 Issue: 2 |