Thiamin absorption by small intestine.

In different animal species, including man, thiamin is absorbed in vivo from the small intestine by means of two mechanism: at low intraluminal concentrations (less than 1.5 microM), absorption shows a saturation kinetics; at higher concentrations, passive transport (diffusion) takes place. The absorption is maximal in the duodenum, its rate decreasing caudally along the small intestine. In vitro at low concentrations, the transcellular transport system of thiamin shows the following general features: it takes place against a chemical concentration gradient, is easily saturable (Km = 0.16-0.63 microM; Vmax = 5.2 mumol X g-1 X h-1), is blocked by cellular metabolic inhibitors, anoxia, low temperature and thiamin structural analogues. It is Na+-dependent and operates mainly from mucosa to serosa. In contrast, distinctive features of the thiamin transfer are the following: entry in the enterocyte in the free form (sodium-independent); pyrophosphorylation by means of a cytoplasm thiamin-pyrophosphokinase; the dephosphorylation of thiamin-pyrophosphate by means of particulate intracellular phosphatases; the cellular exit mainly in the free form, through the action of the controluminal Na-K activated ATPase. A working scheme for thiamin intestinal transport is proposed and discussed.