In food, thiamin occurs mainly as phosphate coen-zymes and the predominant form is TDP (also called thiamin pyrophosphate and cocarboxylase). The phosphate coenzymes are broken down in the gut by phosphatases to give free thiamin for absorption. Thiamin is absorbed mainly from the upper intestine, and less thiamin is absorbed on an empty stomach than when taken with a meal. The latter could be due to the alkaline conditions in the duodenum, which are prevented by the presence of food.
Absorption of up to 2 mg per meal occurs by an active saturable process involving a sodium-dependent adenosine triphosphatase and against a concentration gradient. During absorption, thiamin is phosphorylated to the monophosphate ester (TMP). Thiamin is absorbed via the portal venous system. Further phosphorylation to TDP occurs on entry into all tissues. TDP can cross the blood-brain barrier, where a portion is converted to TTP, although even in the brain, TDP is the predominant form of thiamin. A second passive absorption process operates when intakes of thiamin are >5 mg but the maximum that can be absorbed from an oral dose is 2-5 mg.
The active process of absorption is impaired by ethyl alcohol. For example, 55% of a 5 mg dose of orally administered, labeled thiamin was recovered over 72 h in healthy adults, but this was reduced by 25-40% if they were previously given 1.5-2 g alcohol/kg. In people with fatty livers who had previously been abusing alcohol, mean thiamin absorption was reduced by 60%. However, the passive absorption of thiamin is not inhibited by alcohol, nor does it block entry of thiamin into the liver or interfere with thiamin metabolism in the tissues. Absorption of thiamin may also be reduced by gastrointestinal disturbances, such as vomiting and diarrhea, ulcerative colitis, and neoplasia, and in patients with hepatic disease and achlorhydria.
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