Abstract
The aim of the current study was to evaluate the role of γ-amino butyric acid (GABA) in insulin disturbance and hyperglycemia associated with brain oxidative damage in streptozotocin-treated rats. Streptozotocin (STZ) was administered to male albino rats as a single intraperitoneal dose (60mg/kg body weight). GABA (200mg/Kg body weight/day) was administered daily via gavages during 3weeks to STZ-treated-rats. Male albino rats Sprague-Dawley (10±2weeks old; 120±10g body weight) were divided into 4 groups of 6 rats and treated in parallel. (1) Control group: received distilled water, (2) GABA group: received GABA, (3) STZ group: STZ-treated rats received distilled water, (4) STZ+GABA group: STZ-treated rats received GABA. Rats were sacrificed after a fasting period of 12h next last dose of GABA. The results obtained showed that STZ-treatment produced hyperglycemia and insulin deficiency (similar to type1 Diabetes). These changes were associated with oxidative damage in brain tissue and notified by significant decreases of superoxide dismutase and catalase activities in parallel to significant increases of malondialdehyde and advanced oxidation protein products levels. The histopathology reports also revealed that STZ-treatment produced degeneration of pancreatic cells. The administration of GABA to STZ-treated rats preserved pancreatic tissue with improved insulin secretion, improved glucose level and minimized oxidative stress in brain tissues. It could be concluded that GABA might protect the brain from oxidative stress and preserve pancreas tissues with adjusting glucose and insulin levels in Diabetic rats and might decrease the risk of neurodegenerative disease in diabetes.
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