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      Zinc and Skin Disorders

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          Abstract

          The skin is the third most zinc (Zn)-abundant tissue in the body. The skin consists of the epidermis, dermis, and subcutaneous tissue, and each fraction is composed of various types of cells. Firstly, we review the physiological functions of Zn and Zn transporters in these cells. Several human disorders accompanied with skin manifestations are caused by mutations or dysregulation in Zn transporters; acrodermatitis enteropathica (Zrt-, Irt-like protein (ZIP)4 in the intestinal epithelium and possibly epidermal basal keratinocytes), the spondylocheiro dysplastic form of Ehlers-Danlos syndrome (ZIP13 in the dermal fibroblasts), transient neonatal Zn deficiency (Zn transporter (ZnT)2 in the secretory vesicles of mammary glands), and epidermodysplasia verruciformis (ZnT1 in the epidermal keratinocytes). Additionally, acquired Zn deficiency is deeply involved in the development of some diseases related to nutritional deficiencies (acquired acrodermatitis enteropathica, necrolytic migratory erythema, pellagra, and biotin deficiency), alopecia, and delayed wound healing. Therefore, it is important to associate the existence of mutations or dysregulation in Zn transporters and Zn deficiency with skin manifestations.

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          PPARγ agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein.

          Brown adipose tissue dissipates energy through heat and functions as a defense against cold and obesity. PPARγ ligands have been shown to induce the browning of white adipocytes; however, the underlying mechanisms remain unclear. Here, we show that PPARγ ligands require full agonism to induce a brown fat gene program preferentially in subcutaneous white adipose. These effects require expression of PRDM16, a factor that controls the development of classical brown fat. Depletion of PRDM16 blunts the effects of the PPARγ agonist rosiglitazone on the induced brown fat gene program. Conversely, PRDM16 and rosiglitazone synergistically activate the brown fat gene program in vivo. This synergy is tightly associated with an increased accumulation of PRDM16 protein, due in large measure to an increase in the half-life of the protein in agonist treated cells. Identifying compounds that stabilize PRDM16 protein may represent a plausible therapeutic pathway for the treatment of obesity and diabetes. Copyright © 2012 Elsevier Inc. All rights reserved.
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            Zinc finger proteins: new insights into structural and functional diversity

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              Genome-wide association study in alopecia areata implicates both innate and adaptive immunity.

              Alopecia areata (AA) is among the most highly prevalent human autoimmune diseases, leading to disfiguring hair loss due to the collapse of immune privilege of the hair follicle and subsequent autoimmune attack. The genetic basis of AA is largely unknown. We undertook a genome-wide association study (GWAS) in a sample of 1,054 cases and 3,278 controls and identified 139 single nucleotide polymorphisms that are significantly associated with AA (P
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                11 February 2018
                February 2018
                : 10
                : 2
                : 199
                Affiliations
                Department of Dermatology, Faculty of Medicine, University of Yamanashi, Yamanashi 409-3898, Japan; mkinoshita@ 123456yamanashi.ac.jp (M.K.); sshimada@ 123456yamanashi.ac.jp (S.S.); tkawa@ 123456yamanashi.ac.jp (T.K.)
                Author notes
                [* ]Correspondence: yogawa@ 123456yamanashi.ac.jp ; Tel./Fax: +81-155-273-6766
                Author information
                https://orcid.org/0000-0003-2635-888X
                Article
                nutrients-10-00199
                10.3390/nu10020199
                5852775
                29439479
                ae9d0b39-1ded-413c-a08c-c41489621862
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 07 December 2017
                : 09 February 2018
                Categories
                Review

                Nutrition & Dietetics
                zinc,skin,acrodermatitis enteropathica,langerhans cells,atp,nutrition
                Nutrition & Dietetics
                zinc, skin, acrodermatitis enteropathica, langerhans cells, atp, nutrition

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