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Published on: February 3, 2016
Defective intestinal amino acid absorption in Ace2 null mice
Dustin Singer1, Simone M R Camargo, Tamara Ramadan
1Institute of Physiology, University of Zurich, Switzerland.
Summary
Mice lacking Ace2, crucial for intestinal amino acid transporter B(0)AT1 expression, showed altered amino acid levels but no niacin deficiency or pellagra symptoms, even on a deficient diet.
Area of Science:
- Physiology
- Biochemistry
- Genetics
Background:
- Hartnup disorder, caused by mutations in the neutral amino acid transporter B(0)AT1 (Slc6a19), leads to neutral aminoaciduria and potential pellagra-like symptoms due to impaired L-tryptophan absorption.
- Ace2 is essential for the intestinal expression of B(0)AT1, suggesting a role for Ace2 in amino acid transport and related health conditions.
Purpose of the Study:
- To investigate the impact of intestinal B(0)AT1 absence, mediated by Ace2 deficiency, on amino acid homeostasis and niacin status in mice.
- To determine if Ace2 null mice exhibit symptoms of niacin deficiency or pellagra under dietary challenges.
Main Methods:
- Studied ace2 null mice to assess intestinal B(0)AT1 function and amino acid absorption.
- Measured Na(+)-dependent amino acid uptake in intestinal rings and analyzed luminal and plasma amino acid concentrations.
- Challenged mice with a low-protein, low-niacin diet to evaluate their response and susceptibility to pellagra-like symptoms.
Main Results:
- Ace2 null mice exhibited decreased weight gain and defective Na(+)-dependent uptake of B(0)AT1 substrates, including L-tryptophan.
- Significant increases in ileal L-tryptophan and other neutral amino acids were observed in ace2 null mice, indicating malabsorption.
- Despite altered plasma and muscle amino acid levels, ace2 null mice did not develop niacin deficiency or pellagra symptoms under dietary stress.
Conclusions:
- Ace2-dependent intestinal amino acid transport is critical for efficient absorption of neutral amino acids like L-tryptophan.
- Mice lacking Ace2-dependent transport show significant alterations in amino acid homeostasis but are surprisingly resistant to niacin deficiency and pellagra.
- This suggests compensatory mechanisms or alternative pathways may protect against pellagra in the absence of normal intestinal amino acid transport.
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