Abstract

Type II diabetes affects 37.2 million Americans, with 96 million more affected by pre-diabetes, a condition that could lead to diabetes without lifestyle changes. Metformin, a small molecule biguanide drug, is the first-line treatment for Type II diabetes; however, its mechanism of action is not fully understood. Thiamine (vitamin B1) is a cofactor for enzymes involved in the TCA cycle and pentose-phosphate pathways relevant to glucose metabolism. Data from our lab suggests a correlation between the efficacy of metformin and these thiamine-mediated processes. To study the expression of thiamine-dependent enzymes and transporters in human blood, methods are under development to understand the impact of metformin on thiamine uptake, thiamine’s conversion to active phosphorylated forms, and its cellular retention in human blood from patients who are and are not taking metformin. This work will aid in developing future diabetes treatments and establishing a more complete mechanism of action for metformin.