Figure 8.

Prolonged treatment with clinically relevant concentrations of metformin inhibited oxygen consumption rate (OCR) and increased ATP production through enhancement of glycolysis pathway in vitro. Primary astrocytes (A) and primary neurons (B) were treated with metformin (20 µM and 200 µM) for 24 hours before seahorse extracellular flux analysis; bar graph indicated base OCR of each condition (n=6). C) ATP assay in primary astrocyte culture after treatment with 20 µM and 200 µM metformin for 3, 6 and 24 hours (n=6). D) Total ATP in primary astrocytes was increased after 24-hour treatment with 50 µM metformin. Astrocyte was treated with 10 mg/ml oligomycin for 2 hours to inhibit ATP production from mitochondrial oxidative phosphorylation. Lactate production was increased by metformin treatment (n=6). E) Total ATP (24-hour treatment) and ATP from glycolysis (2-hour treatment) in primary neurons were increased by 50 µM metformin treatment (n=6) (* p<0.05).