Fig. 1.

The effects of benfotiamine on a [U-¹⁴C]glucose oxidation (CO₂ formation), b total metabolized glucose (sum of CO₂ formation and cell-associated glucose) and c fractional oxidation of [U-¹⁴C]glucose (CO₂/sum of cell-associated plus CO₂) under NG (normoglycemic, 5.5 mM glucose) and HG (hyperglycemic, 20 mM glucose) conditions. Myotubes were treated for 4 days in the absence or presence of benfotiamine (100 and 200 μM) under NG and HG conditions. All data are normalized to normoglycemic control and presented as mean ± SEM (n = 5 for NG and n = 3 for HG, independent muscle cell donors). ^aP < 0.05 versus control myotubes not exposed to benfotiamine under NG conditions; ^bP < 0.05 versus control myotubes not exposed to benfotiamine under HG conditions (linear mixed model (LMM), SPSS). HG treatment significantly decreased glucose oxidation and total metabolized glucose (P < 0.001 overall effect) (LMM). d Dose–response effects of benfotiamine on [U-¹⁴C]glucose oxidation (CO₂ formation) under NG conditions (mean ± SEM, n = 2)