Key result
Ace2 deficiency in mice resulted in highly increased susceptibility to intestinal inflammation, driven by altered gut microbial ecology and impaired dietary amino acid homeostasis.
Population
Murine models including angiotensin I converting enzyme 2 (Ace2) deficient mice and germ-free wild-type hosts
Comparison
Ace2 deficiency; dietary tryptophan and… vs Wild-type mice
Design
Preclinical
Authors
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Ace2-microbiome links in mice may inform IBD mechanisms; hypothesis-generating for human translation.
ACE2 has a RAS-independent function in regulating intestinal amino acid homeostasis and the gut microbiome, explaining how protein malnutrition can lead to intestinal inflammation.
Hashimoto et al. (2012) studied Intestinal inflammation and colitis. Ace2 deficiency vs. Wild-type was evaluated on Susceptibility to intestinal inflammation. Ace2 deficiency in mice resulted in highly increased susceptibility to intestinal inflammation, driven by altered gut microbial ecology and impaired dietary amino acid homeostasis.
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