Absorption of Zinc in Acrodermatitis Enteropathica

Lombeck, I.; Schnippering, Holger; Ritzl, F.; Feinendegen, L. E.; Bremer, H. J.

doi:10.1016/s0140-6736(75)93025-1

Cited by 117 publications

(40 citation statements)

References 9 publications

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“…nutrient zinc transport; absorption; transcription; gene regulation SEVERAL MUTATIONS of the Slc39a4 gene (Zip4) produce acrodermatitis enteropathica in humans (23,33). Acrodermatitis enteropathica patients have low intestinal zinc absorption and severe zinc deficiency, including secondary cutaneous infections, as well as other manifestations of zinc deprivation (19,22,24,31). The demonstration that pathological signs abate in acrodermatitis enteropathica patients upon zinc supplementation (22,24,31) suggests that ZIP4 is a major zinc transporter in the gastrointestinal tract responsible for adequate zinc balance and homeostasis in humans.…”

mentioning

confidence: 99%

Krüppel-like factor 4 regulates adaptive expression of the zinc transporterZip4in mouse small intestine

Liuzzi

Guo²,

Chang³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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mentioning

confidence: 99%

Krüppel-like factor 4 regulates adaptive expression of the zinc transporterZip4in mouse small intestine

Liuzzi

Guo²,

Chang³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…The primary basis of AE is hypothesized to be the reduced uptake of dietary zinc by intestinal cells (15,16) because patients respond positively to dietary zinc supplements (11,12,17,18). Consistent with this hypothesis was the finding that the affected protein in AE, hZIP4, and the murine homolog, mZIP4, are most abundantly expressed in the small intestine (8), and the mZIP4 protein is located at the apical membrane of intestinal enterocytes in zinc-deficient mice (8,19).…”

mentioning

confidence: 99%

Zn2+-stimulated Endocytosis of the mZIP4 Zinc Transporter Regulates Its Location at the Plasma Membrane

Kim

Wang

Dufner-Beattie

et al. 2004

Journal of Biological Chemistry

142

136

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Zinc is an essential nutrient for all organisms. Its requirement in humans is illustrated dramatically by the genetic disorder acrodermatitis enteropathica (AE). AE is caused by the reduced uptake of dietary zinc by enterocytes, and the ensuing systemic zinc deficiency leads to dermatological lesions and immune and reproductive dysfunction. The gene responsible for AE, SLC39A4, encodes a member of the ZIP family of metal transporters, hZIP4. The mouse ZIP4 protein, mZIP4, stimulates zinc uptake in cultured cells, and studies in mice have demonstrated that zinc treatment decreases mZIP4 mRNA levels in the gut. In this study, we demonstrated using transfected cultured cells that the mZIP4 protein is also regulated at a post-translational level in response to zinc availability. Zinc deficiency increased mZIP4 protein levels at the plasma membrane, and this was associated with increased zinc uptake. Significantly, treating cells with low micromolar zinc concentrations stimulated the rapid endocytosis of the transporter. Zinc-regulated localization of the human ZIP4 protein was also demonstrated in cultured cells. These findings suggest that zinc-regulated trafficking of human and mouse ZIP4 is a key mechanism controlling dietary zinc absorption and cellular zinc homeostasis.

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“…Acrodermatitis enteropathica exacerbation during pregnancy or the stress of disease may require an increase in therapy. Warm compresses to remove the scale crust, followed by application of white petrolatum to eroded skin lesions, may enhance reepithelialization when used concurrently with zinc replacement [17]. Genetic counseling is recommended for families of patients with the congenital form of acrodermatitis enteropathica.…”

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confidence: 99%

A study on efficacy of oral zinc therapy for treatment of acrodermatitis enteropathica

Puri¹,

Puri²

2013

Our Dermatol Online

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Introduction: Acrodermatitis enteropathica (AE) is a disorder of zinc metabolism that occurs in one of two forms: an inborn (congenital) form and an acquired form. The inborn form of AE is a rare genetic disorder characterized by intestinal abnormalities that leads to inability to absorb zinc from the intestine. The lack of zinc presents, characteristically, as skin inflammation with pustules occurring around the mouth and/or anus, diarrhea. Aims: To study the efficacy of oral zinc therapy on thirty patients of acrodermatitis enteropathica. Methods: Thirty clinically diagnosed patients of acrodermatitis enteropathica were taken for the study. The criterion of diagnosis of this condition was the clinical picture of symmetrical vesiculo-pustular dermatitis, in upper and lower limbs and periorificial regions. Results and Discussion: In our study maximum (50%) patients were below 1 year of age, 33.3% patients were between 13-24 months of age, 6.66% patients were between 25-36 months and 37-48 months each and 3.33% patients were between 49-60 months of age. Nail changes were seen in 60% children. Also, it was seen that perioral area was the commonest (86.6%) site involved, followed by anogenital area in 80% patients, palms and soles were involved in 66.6% patients, arms in 46.6% patients and legs were seen in 40% patients. Regarding clinical features, dermatitis was seen in 100%patients, alopecia was seen in 40% patients, diarrhea in 60% patients and mental disturbances were seen in 30 % patients.

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Absorption of Zinc in Acrodermatitis Enteropathica

Cited by 117 publications

References 9 publications

Krüppel-like factor 4 regulates adaptive expression of the zinc transporterZip4in mouse small intestine

Krüppel-like factor 4 regulates adaptive expression of the zinc transporterZip4in mouse small intestine

Zn2+-stimulated Endocytosis of the mZIP4 Zinc Transporter Regulates Its Location at the Plasma Membrane

A study on efficacy of oral zinc therapy for treatment of acrodermatitis enteropathica

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