Abstract: Thiamine (vitamin B1) is a water-soluble and essential vitamin and act as a coenzyme after converting to thiamine pyrophosphate in crucial metabolic enzymes of pyruvate dehydrogenase, α-ketoglutarate dehydrogenase and transketolase. The original paper that investigated the influence of stepwise increases in carbohydrate intake on thiamine requirement seems to mislead the reader into considering an increase in thiamine requirement for excessive carbohydrate intake. Thiamine is reabsorbed in the brush border membrane of renal proximal tubular cells through thiamine transporters. The transport of thiamine with a stoichiometric thiamin/H+ exchange of 1:1 is facilitated by the outward H+ gradient and the low thiamine intracellular concentration maintained by its rapid conversion to thiamine pyrophosphate. The thiamine reabsorption is affected by the activity of Na+/H+ exchanger 3 secreting H+ for the acidification of tubular fluid. The exit of thiamine into an interstitial fluid is coupled directly to the hydrolysis of ATP in sodium pump. The activity of Na+/H+ exchanger 3 has been demonstrated to be enhanced in diabetic patients and suppressed by sodium-glucose co-transporter 2 inhibitors. Excessive glucose reabsorption is presumed to inhibit the thiamin reabsorption in the proximal tubule, leading to an increase in urinary thiamine excretion as demonstrated in diabetic patients. Thiamine supplementation would not be required only for a carbohydrate-rich diet while keeping in mind the thiamine bioavailability and metabolism in the body. Further studies are needed to clarify the relationship between excessive carbohydrate intake and thiamine requirement.