What question did this study set out to answer?

Investigate the cellular and physiological consequences of enterocyte-specific ZIP4 deficiency to elucidate the pathogenesis of acrodermatitis enteropathica.

June 21, 2012PLoS GeneticsOpen Access

A Mouse Model of Acrodermatitis Enteropathica: Loss of Intestine Zinc Transporter ZIP4 (Slc39a4) Disrupts the Stem Cell Niche and Intestine Integrity

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Authors

JGJim GeiserUniversity of Kansas Medical Center KVKoen J. T. VenkenBaylor College of Medicine RLRobert C. De LisleUniversity of Kansas Medical Center

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Implication

Animal study reveals that enterocyte ZIP4 loss impairs Paneth cell function and nutrient absorption in mice, highlighting mechanisms underlying lethal acrodermatitis enteropathica.

Key Points

Investigate the cellular and physiological consequences of enterocyte-specific ZIP4 deficiency to elucidate the pathogenesis of acrodermatitis enteropathica.
Generated a tamoxifen-inducible, enterocyte-specific Zip4 (Slc39a4) knockout mouse model mimicking acrodermatitis enteropathica.
Assessed intestinal crypt architecture, cell division, Paneth cell differentiation markers (Sox9, lysozyme, mucin), and villus enterocyte mTOR1 signaling.
Quantified trace metal concentrations (zinc, iron, manganese, copper) across the small intestine, liver, and pancreas under normal and zinc-supplemented feeding.
Inducible knockout of intestinal Zip4 caused severe wasting and death, which was completely prevented by lactation or high dietary zinc supplementation.
ZIP4 deletion rapidly depleted Paneth cell labile zinc, reduced Sox9 and lysozyme expression, induced abnormal mucin accumulation, decreased crypt cell division, and attenuated enterocyte mTOR1 activity.
Small intestine, liver, and pancreas total zinc levels decreased sharply, while iron, manganese, and copper progressively accumulated in hepatic tissue.

Cite This Study

Geiser et al. (2012) studied this question.

synapsesocial.com/papers/69dea57557c7c8340a558f3d https://doi.org/10.1371/journal.pgen.1002766

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Implication

Animal study reveals that enterocyte ZIP4 loss impairs Paneth cell function and nutrient absorption in mice, highlighting mechanisms underlying lethal acrodermatitis enteropathica.

A Mouse Model of Acrodermatitis Enteropathica: Loss of Intestine Zinc Transporter ZIP4 (Slc39a4) Disrupts the Stem Cell Niche and Intestine Integrity

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Cite This Study

A Mouse Model of Acrodermatitis Enteropathica: Loss of Intestine Zinc Transporter ZIP4 (Slc39a4) Disrupts the Stem Cell Niche and Intestine Integrity

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