Submitted to: Gastroenterology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/8/1995
Publication Date: N/A
Citation: N/A Interpretive Summary: In the past, the only known source of the B-vitamin, folate, for human beings was the diet. Nevertheless, it is well known that several of the bacteria which are normally found in the human intestine can produce folate. The purpose of this study was to determine whether any of the folate produced in the intestine by bacteria is absorbed and utilized by the human host. Two groups of human volunteers who had excessive quantities of bacteria in their intestine were studied for this effect. One group of individuals had a condition called atrophic gastritis, which is common among the aged and which results in a modest increase in bacteria in the small intestine. The second group was healthy and was administered a commonly prescribed drug which blocks acid secretion by the stomach and thereby causes an increase in small intestinal bacteria. A narrow, hollow tube was placed through the nose of each individual and fed into the small intestine. Juice from the small intestine revealed high concentrations of bacteria: when the bacteria in this juice were incubated outside the body they produced a lot of folate. A slightly read- ily detectable form of a specialty nutrient, which bacteria use to produce folate, was then introduced into the small intestine of the subjects. Readily dectectable folate was produced in the intestine, and was subse- quently absorbed by the human subjects. Subjects with atrophic gastritis and those who had been treated with the drug excreted significantly more bacterially created folate in the urine than the healthy subjects who had not received the drug. This study demonstrates that folate created in the small intestine is taken up by the human host, and incorporated into the body stores of folate.
Technical Abstract: Some intestinal flora are known to synthesize folate. The aim of this study was to determine whether folate synthesized by small intestinal flora is assimilated by the human host. Subjects with atrophic gastritis and healthy volunteers wee studied before and after omeprazole administration. A double-lumen perfusion tube was placed in the duodenum. 3H-labeled P-aminobenzoic acid, a precursor substrate for bacterial folate synthesis, was perfused. Downstream intestinal aspirates and a 48-hour urine collection were obtained. Atrophic gastritis and omeprazole administration were associated with increases in duodenal pH and in small intestinal flora. Bacterially synthesized folates were isolated from the intestinal aspirates. Tritiated 5- methyltetrahydrofolate, a major metabolite of folate, was isolated from the urine of omeprazole-treated subjects (P<0.01). The quantity of tritiated 5-methyltetrahydrofolate in the urine of subjects with atrophic gastritis was similarly elevated. Mild bacterial over-growth caused by atrophic gastritis and administration of omeprazole are associated with de novo folate synthesis in the lumen of the small intestine; the human host absorbs and uses some of these folates; and the contribution to folate nutriture from this source remains unclear.