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dc.contributor.authorKroupina, Katerina
dc.contributor.authorBémeur, Chantal
dc.contributor.authorRose, Christopher
dc.subjectAmino acidsfr
dc.subjectHepatic encephalopathyfr
dc.titleAmino acids, ammonia, and hepatic encephalopathyfr
dc.contributor.affiliationUniversité de Montréal. Faculté de médecine. Département de médecinefr
dc.contributor.affiliationUniversité de Montréal. Faculté de médecine. Département de nutritionfr
dc.contributor.affiliationUniversité de Montréal. Faculté de médecine. Département de pharmacologie et physiologiefr
dcterms.abstractHepatic encephalopathy (HE) is a decline in brain function arising due to liver insufficiency. The liver's diminished capacity to clear ammonia, and the subsequent accumulation of it, is highly implicated in pathogenesis of HE. Ammonia is endogenously generated from the catabolism of amino acids derived from dietary protein intake. Therefore, a conflict arises in cirrhosis where dietary protein intake may increase ammonia and precipitate HE, and at the same time, cirrhotic patients require high daily protein intake due to altered nutrient metabolism. A nutritional solution is needed to deliver sufficient doses of protein to patients without increasing the risk of HE. In order to address this issue, this review will discuss the catabolism of individual amino acids with a special focus on ammonia-generating steps and highlight a subset of amino acids that have the potential to generate multiple equivalents of ammonia. Following, studies investigating the effects of individual amino acids in cirrhosis on blood ammonia levels as well as development of HE will be
UdeM.VersionRioxxVersion acceptée / Accepted Manuscriptfr
oaire.citationTitleAnalytical biochemistryfr

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