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The degradation of amino acids, proteins, and blood to short-chain fatty acids in colon is prevented by lactulose.

Abstract：

:Short-chain (C2-C5) fatty acids account for 60%-70% of the anions in the colon. Acetate (C2) is nontoxic in contrast to C(3)4-C5 fatty acids (propionate, butyrate, isobutyrate, valerate, and isovalerate), which induce coma in animals and may be important in the pathogenesis of hepatic coma in humans. An in-vitro fecal incubation system was used to map out short-chain fatty acid production in the presence of lactulose, amino acids, albumin, or blood. Albumin and blood increased production of all C2-C5 fatty acids. In contrast, lactulose was converted to acetate only and increased fecal acidity. The degradation of amino acids, albumin, and blood to short-chain fatty acids was completely inhibited by 10-25 mM lactulose. This was caused mainly by the acidifying effect of lactulose. pH-independent inhibition of blood and amino acid degradation to short-chain fatty acids required concentrations of lactulose exceeding 50-100 mM. Thus, the effect of lactulose in the treatment of hepatic coma may be related to its rapid fermentation into organic acids at rates exceeding colonic buffering capacity. This probably reduces formation of toxic fatty acids and ammonia from amino acids, polypeptides, and blood in the colon.

journal_name

Gastroenterology

journal_title

Gastroenterology

authors

Mortensen PB,Holtug K,Bonnén H,Clausen MR

doi

10.1016/0016-5085(90)90825-l

subject

Has Abstract

pub_date

1990-02-01 00:00:00

pages

353-60

issue

2

eissn

0016-5085

issn

1528-0012

pii

0016-5085(90)90825-L

journal_volume

98

pub_type

杂志文章

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