Endocrine Abstracts

Objective: Bacalin was known as an allosteric modulator of the benzodiazepine sites of the γ-aminobutyric acid A receptor (GABA_AR), which produce anxiolytic effects in mice without myorelaxant or sedative effects. Baicalin occur flavonoid found in naturally in the genus Scutellaria. It has been recently shown to exert metabolic effects by attenuating hyperglycemia-induced mitochondrial damage in β-cells in diabetic rats, high-fat diet- (HFD-) induced body weight gain, and lipid deposits in the liver and systemic inflammation in mice. This study investigated the effects of baicalin on islet functions and diabetic status in HFD-induced obese diabetic mice.

Methods: C57BL/6 mice were grouped into normal control, HF control, HF sham, and 4 different baicalin dose-administered groups (25, 50, 100, and 150 mg/kg). HFD containing 60% fat and water were fed ad libitum for 24 weeks. Designated doses of baicalin or 0.9% saline were administered intraperitoneally 5d/wk. Body weight (BW) and conventional glucose homeostasis parameters (FPG, FPI, AUC-glucose, AUC-insulin, and etc.) were monitored; in addition, ex vivo glucose-stimulated insulin secretion (GSIS) and glucagon secretion (GSGS) with isolated islets were performed.

Results: Insulin secretion in response to high glucose stimulation (16.7 mM) was significantly higher in islets isolated from the groups administered 50, 100, 150 mg/kg baicalin compared to HF control; glucagon secretion was significantly suppressed by high glucose stimulation in islets from the same groups.

Conclusion: This study showed that baicalin had positive effects on glycemic control by regulating secretion of insulin and glucagon, possibly through GABA_AR mediation.