International Journal of Celiac Disease
ISSN (Print): 2334-3427 ISSN (Online): 2334-3486 Website: https://www.sciepub.com/journal/ijcd Editor-in-chief: Samasca Gabriel
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International Journal of Celiac Disease. 2022, 10(1), 8-10
DOI: 10.12691/ijcd-10-1-6
Open AccessArticle

Molecular Mechanisms of Zinc Absorption in Health, Acrodermatitis Enteropathica and Celiac Disease

Hugh James Freeman1,

1Department of Medicine (Gastroenterology), University of British Columbia, Vancouver, BC, Canada

Pub. Date: September 05, 2022

Cite this paper:
Hugh James Freeman. Molecular Mechanisms of Zinc Absorption in Health, Acrodermatitis Enteropathica and Celiac Disease. International Journal of Celiac Disease. 2022; 10(1):8-10. doi: 10.12691/ijcd-10-1-6

Abstract

Zinc is an essential trace element involved in a multitude of human biological processes. Normally, zinc homeostasis is largely maintained by uptake of zinc into the enterocyte involving the brush border membrane followed by baso-lateral membrane exit into the circulation. This is accomplished by distinct gene-based protein carriers (eg., ZIP4, ZnT-1) to balance zinc loss, particularly from the intestinal and urinary tracts as well as integument. A genetically-based autosomal recessive disorder, acrodermatitis enteropathica, and other disorders leading to secondary malabsorption of zinc, such as celiac disease, may alter this balance, lead to significant dermatologic and intestinal histological effects, but may be entirely reversible with oral zinc supplements. Importantly, zinc may also attenuate transglutaminase activities and has been suggested to have the potential, hypothetically, to promote the generation of “celiac-safe” products.

Keywords:
zinc ZIP4 microvillus membrane transporter ZnT-1 basolateral membrane transporter enterocyte zinc homeostasis acrodermatitis entero pathica zinc absorption and malabsorption

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References:

[1]  King JC. Zinc: an essential bu elusive nutrient. Am J Clin Nutr 2011; 94: 6795-6845.
 
[2]  Maret W. Zinc in cellular regulation. The nature and significance of “zinc signals”. Int J Mol Sci 2017; 18: 2285.
 
[3]  Krebs NF. Overview of zinc absorption and excretion in the human gastrointestinal tract. J Nutr 2000; 130: 1374S-1377S.
 
[4]  Hambidge KM, Miller LV, Westcott JE, Sheng X, Krebs NF. Zinc bioavailability and homeostasis. Am J Clin Nutr 2010; 91: 1478S-1483S.
 
[5]  Steinhardt HJ, Alibi SA. Interaction between transport of zinc and other solutes in human intestine. Am J Physiol 1984; 247: G176-G182.
 
[6]  Lee HH, Prasad AS, Brewer GJ, Owyang C. Zinc absorption in human small intestine. Am J Physiol 1989; 256: G87-G91.
 
[7]  Maares M, Haase H. A guide to human zinc absorption: general overview and recent advances of in vitro intestinal models. Nutrients 2020; 12: 762.
 
[8]  Kury S, Dreno B, Bezieau S, Giraudet S, Kharfi M, Kamoun R, Moisan JP. Identification of slc39a4, a gene involved in acrodermatitis enteropathica. Nat Genet 2002; 31: 239-240.
 
[9]  Wang K, Zhou B, Kuo YM, Zemansky J, Gitschier J. A novel member of a zinc transporter family is defective in acrodermatitis enteropathica. Am J Hum Genet 2002; 71: 66-73.
 
[10]  Wang F, Kim BE, Petris MJ, Eide DJ. The mammalian zip5 protein is a zinc transporter that localizes to the basolateral surface of polarized cells. J Biol Chem 2004; 279: 51433-51441.
 
[11]  Guthrie GJ, Aydemir TB, Troche C, Martin AB, Chang SM, Cousins RJ. Influence of zip14 (slc39a14) on intestinal zinc processing and barrier function. Am J Physiol Gastrointest Liver Physiol 2015; 308: G171-G1778.
 
[12]  Graves K, Kestenbaum T, Kalivas J. Hereditary acrodermatitis enteropathica in an adult. Arch Dermatol 1980; 116: 562-564.
 
[13]  Ogawa Y, Kinoshita M, Shimada S, Kawamura T. Zinc and skin disorders. Nutrients 2018; 10.
 
[14]  Ciampo IR, Sawamura R, Ciampo LA, Fernandes MI. Acrodermatitis enteropathica: clinical manifestations and pediatric diagnosis. Rev Paul Pediatr 2018; 36: 238-241.
 
[15]  Lewin KJ, Riddell RH, Weinstein WM. Gastrointestinal Pathology and its Clinical Implications Volume II. Igaku-Shoin, Tokyo. 1992; 778.
 
[16]  Kelly R, Davidson GP, Townley RR, Campbell PE. Reversible intestinal mucosal abnormality in acrodermatitis enteropathica. Arch Dis Child 1976; 51: 219-222.
 
[17]  Neldner KH, Hagler L, Wise WR, Stifel FB, Lufkin EG, Herman RH. Acrodermatitis enteropathica. Arch Dermatol 1974; 110:711.
 
[18]  Ament ME, Broviac J. Acrodermatitis enteropathica: demonstration of small and large intestinal mucosal lesions: failure of hyperalimentation, Intralipid and Diodoquin to reverse the intestinal lesions and generalized malabsorption syndrome. Gastroenterology 1973; 64: 692.
 
[19]  Bohane TD, Cutz E, Hamilton JR, Gall DG. Acrodermatitis enteropathica, zinc, and the Paneth cell. A case report with family studies. Gastroenterology 1977; 73: 587-592.
 
[20]  Singhai N, Alam S, Sherwani R, Musarrat J. Serum zinc levels in celiac disease. Indian Pediatr 2008; 45: 319-321.
 
[21]  Erdem T, Ferat C, Nurdan YA, Halime E, Selcuk SM, Hamza K, Ayse SM. Vitamin and mineral deficiency in children newly diagnosed with celiac disease. Turk J Med Sci 2015; 45: 833-836.
 
[22]  Tran CD, Katsikeros R, Manton N, Krebs NF, Hambridge KM,Butler RN, Davidson GP. Zinc homeostasis and gut function in children with celiac disease. Am J Clin Nutr 2011; 94: 1026-1032.
 
[23]  Crofton RW, Glover SC, Ewen SW, Aggett PJ, Mowat NA, Mills CF. Zinc absorption in celiac disease and dermatitis herpetiformis: a test of small intestinal function. Am J Clin Nutr 1983; 38: 708-712.
 
[24]  Rawal P, Thapa BR, Prasad R, Prasad KK, Nain CK, Singh K. Zinc supplementation to patients with celiac disease—is it required? J Trop Pediatr 2010; 56: 391-397.
 
[25]  Negi K, Kumar R, Sharma L, Datta SP, Choudhury M, Kumar P. Serum zinc, copper and iron status of children with celiac disease on three months of gluten-free diet with or without four weeks of zinc supplements: a randomized controlled trial. Trop Doct 2018; 48: 112-116.
 
[26]  Freeman HJ. Iron refractory or iron resistant iron deficiency anemia in adult celiac disease resolves with a gluten-free diet. Inter J Celiac Dis 2018; 6: 26-29.
 
[27]  Stenberg P, Roth B, Ohlsson B. Zinc as a modulator of transglutaminase activity—laboratory and pathophysiological aspects. J Transl Autoimmun 2021; 4: 100110.
 
[28]  Roth EB, Sjoberg K, Stenberg P. Biochemical and immuno-pathological aspects of tissue transglutaminase in celiac disease. Autoimmunity 2003; 36: 221-226.
 
[29]  Sardy M, Karpati S, Merkl B, Paulsson M, Smyth N. Epidermal transglutaminase (TGase 3) is the autoantigen of dermatitis herpetiformis. J Exp Med 2002; 195: 747-757.
 
[30]  Engstrom N, Saenz-Mendez P, Scheers J, Scheers N. Towards celiac-safe foods: decreasing the affinity of transglutaminase 2 for gliadin by addition of ascorbyl palmitate and ZnCl2 as detoxifiers. Sci Rep 2017; 7: 77.