Colon intestinal bacteria

Substantial individual differences were observed in the response to study breads and the ranges of enterolactone concentration changes in the groups were as follows -54.5-60.0 nmol/1 (placebo), -26.2-101.3 nmol/1 (LP), -19.6-81.8 nmol/1 (HP). This was something that could have been expected as in several studies dietary factors have explained only 10% of the variation in serum enterolactone (Vanharanta et al, 2002b Kilkkinen et al., 2001). This gives further support to the major role of intestinal bacteria in the synthesis of enterolactone. Decreased concentrations of enterolactone may occur due to an increased fiber intake, which may shorten the retention time in the colon and lead to incomplete metabolism of plant lignans. Constipation was earlier shown to be associated with an increased level of serum enterolactone (Kilkkinen et al., 2001). 

The nitrate (NOp content in crops is one of the most important indicators of farm production quality. Nitrate content in food is strictly regulated because of its toxicity, especially in young children. The actual toxin is not the nitrate ion itself but rather the nitrite ion (NOp, which is formed when nitrate is reduced by intestinal bacteria, notably Escherichia coli. In adults, nitrate is absorbed high in the digestive tract before reduction can take place. In infants, whose stomachs are less acidic, E. coli can colonize higher up the digestive tract and therefore reduce the NOJ to NCp before it is absorbed. 

Absorption-The absolute bioavailability of oral sulfasalazine is less than 15% for parent drug. In the intestine, sulfasalazine is metabolized by intestinal bacteria to SP and 5-ASA. Of the two, SP is relatively well absorbed from the colon and highly metabolized with an estimated bioavailability of 60%. 5-ASA is much less well absorbed with an estimated bioavailability of 10% to 30%. Peak plasma levels of both occur approximately 10 hours after dosing. 

Saline laxatives like MgS04, Mg(OH)2, Mg2 Citrate and Na+ Phosphates act via their osmotic pressure to retain water in the colon. Other osmotic laxatives are carbohydrates such as lactulose, glycerin, sorbitol, and mannitol. They are not absorbed and are resistant to digestion in the small intestine. Most agents are orally administered. It should be noted however that glycerin, sodium phosphates and sorbitol are formulated for rectal use. From lactulose lactic and acetic acids are formed by intestinal bacteria and apart from its osmotic effects it thus acidifies the content of the colon. The reduction of the pH stimulates motility and secretion. 

Osmotic laxatives (e.g., lactulose, sorbitol) are poorly absorbed or nonabsorbable compounds that draw additional fluid into the GI tract. Lumen osmolality increases, and fluid movement occurs secondary to osmotic pressure. Lactulose is a synthetic disaccharide that is poorly absorbed from the GI tract, since no mammalian enzyme is capable of hydrolyzing it to its monosaccharide components. It therefore reaches the colon unchanged and is metabolized by colonic bacteria to lactic acid and to small quantities of formic and acetic acids. Since lactulose does contain galactose, it is contraindicated in patients who require a galactose-free diet. Metabolism of lactulose by intestinal bacteria may result in increased formation of intraluminal gas and abdominal distention. Lactulose is also used in the treatment of hepatic encephalopathy. 

Vitamin confers biologic activity upon prothrombin and factors VII, IX, and X by participating in their postribosomal modification. Vitamin is a fat-soluble substance found primarily in leafy green vegetables. The dietary requirement is low, because the vitamin is additionally synthesized by bacteria that colonize the human intestine. Two natural forms exist vitamins Ki and K2. Vitamin K1 (phytonadione Figure 34-5) is found in food. Vitamin K2 (menaquinone) is found in human tissues and is synthesized by intestinal bacteria. 

Sulfasalazine, balsalazide, and olsalazine contain 5-ASA bound by an azo (N=N) bond to an inert compound or to another 5-ASA molecule (Figure 62-8). In sulfasalazine, 5-ASA is bound to sulfapyridine in balsalazide, 5-ASA is bound to 4-aminobenzoyl-B-alanine and in olsalazine, two 5-ASA molecules are bound together. The azo structure markedly reduces absorption of the parent drug from the small intestine. In the terminal ileum and colon, resident bacteria cleave the azo bond by means of an azoreductase enzyme, releasing the active 5-ASA. Consequently, high concentrations of active drug are made available in the terminal ileum or colon. 

Biotin uptake into enterocytes is by a sodium-dependent carrier, which also transports pantothenic acid (Section 12.2) and lipoic acid, but is inhibited by biocytin and dethiobiotin. The carrier is found in both the small intestine and the colon, so both biotin and pantothenic acid synthesized by intestinal bacteria can be absorbed (Chatterjee etal., 1999 Ramaswamy, 1999 Said, 1999 Prasad and Ganapathy, 2000). Even at relatively high intakes (up to 80 /rmol), biotin is more-or-less completely absorbed (Zempleni and Mock, 1999b). 

Prebiotic fiber in fruits is most easily associated with pulp—the fleshy, juicy part of a fruit—as opposed to its edible skin or seed coats which provide insoluble fiber. Prebiotic fiber provides diversified health benefits supporting advantageous intestinal bacteria and immune functions, all of which help deter both the onset of colon cancer and high blood cholesterol levels. 

The answer is c. (Murray, pp 627-661. Scriver, pp 3897—3964. Sack, pp 121-138. Wilson, pp 287-320.) Hemorrhagic disease of the newborn is caused by poor transfer of maternal vitamin K through the placenta and by lack of intestinal bacteria in the infant for synthesis of vitamin K. The intestine is sterile at birth and becomes colonized over the first few weeks. Because of these factors, vitamin K is routinely administered to newborns. Deficiencies of the fat-soluble vitamins A, E, D, and K can occur with intestinal malabsorption, but avid fetal uptake during pregnancy usually prevents infantile symptoms. Hypervltaminosis A can cause liver toxicity but not bleeding, and deficiencies of E (neonatal anemia) or C (extremely rare in neonates) have other symptoms besides bleeding. 

Carbohydrate malabsorption plays a major role in diarrhea associated with SBS. Unabsorbed carbohydrates are broken down by intestinal bacteria to short-chain fatty acids (SCFAs), producing an osmotic load in the distal small intestine and colon that can lead to protracted diarrhea. However, the colon is able to use these SCFAs as a source of energy, thus complex carbohydrates may provide a significant caloric source for patients with a massive resection and a preserved colon. ... 

Bacteria causing gastrointestinal infection need to penetrate the mucus layer before attaching themselves to the epithelial surface. This attachment is usually mediated by bacterial fimbriae or pilus structures, although other cell surface components may also take part in the process. Adherent bacteria colonize intestinal epithelium by multiplication and initiation of a series of biochemical reactions inside the target cell through signal transduction mechanisms (with or without the help of toxins) (51). 

When we are born we are sterile there are no bacteria on or in our bodies. Normally the first thing that happens after birth is that we are placed on our mother s stomach and we begin to nurse. At this moment our skin begins to be colonized with human-friendly bacteria from our mother s body, and our intestinal tract begins to be colonized from bacteria from our mother s milk. 

Arimochi, H., Kinouchi, T., Kataoka, K., Kuwahara, T., and Ohnishi, Y., Effect of intestinal bacteria on formation of azoxymethane-induced aberrant crypt foci in the rat colon, Biochem. Biophys. Res. Commun., 238, 753-757, 1997. 

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