Obesity resistance of the stearoyl-CoA desaturase-deficient (scd1-/-) mouse results from disruption of the epidermal lipid barrier and adaptive thermoregulation

Publikationen: Beitrag in FachzeitschriftZeitschriftenaufsätzeForschung

Standard

Obesity resistance of the stearoyl-CoA desaturase-deficient (scd1-/-) mouse results from disruption of the epidermal lipid barrier and adaptive thermoregulation. / Binczek, Erika; Jenke, Britta; Holz, Barbara; Günter, Robert Heinz; Thevis, Mario; Stoffel, Wilhelm.

in: Biological chemistry, Jahrgang 388, Nr. 4, 01.04.2007, S. 405-418.

Publikationen: Beitrag in FachzeitschriftZeitschriftenaufsätzeForschung

Harvard

APA

Vancouver

Bibtex

@article{3d22af03f6fd43389b4094405534522a,
title = "Obesity resistance of the stearoyl-CoA desaturase-deficient (scd1-/-) mouse results from disruption of the epidermal lipid barrier and adaptive thermoregulation",
abstract = "Targeted deletion of the stearoyl-CoA desaturase 1 gene (scd1) in mouse causes obesity resistance and a severe skin phenotype. Here, we demonstrate that SCD1 deficiency disrupts the epidermal lipid barrier and leads to uncontrolled transepidermal water loss, breakdown of adaptive thermoregulation and cold resistance, as well as a metabolic wasting syndrome. The loss of omega-hydroxylated very long-chain fatty acids (VLCFA) and ceramides substituted with omega-hydroxylated VLCFA covalently linked to corneocyte surface proteins leads to the disruption of the epidermal lipid barrier in scd1-/- mutants. Artificial occlusion of the skin by topical lipid application largely reconstituted the epidermal barrier and also reversed dysregulation of thermogenesis and cold resistance, as well as the metabolic disturbances. Interestingly, SCD1 deficiency abolished expression of the key transcription factor Lef1, which is essential for interfollicular epidermis, sebaceous glands, and hair follicle development. Finally, the occurrence of SCD1 and a newly described hSCD5 (ACOD4) gene in humans suggests that the scd1-/- mouse mutant might be a valuable animal model for the study of human skin diseases associated with epidermal barrier defects.",
keywords = "Administration, Topical, Animals, Body Temperature Regulation, Ceramides, Cholesterol, Cold Temperature, Down-Regulation, Energy Metabolism, Epidermis, Lipids, Liver, Lymphoid Enhancer-Binding Factor 1, Mice, Mice, Knockout, Obesity, Petrolatum, Signal Transduction, Skin Absorption, Skin Diseases, Genetic, Stearoyl-CoA Desaturase, Transcription Factors, Triglycerides, Wasting Syndrome, Water Loss, Insensible",
author = "Erika Binczek and Britta Jenke and Barbara Holz and G{\"u}nter, {Robert Heinz} and Mario Thevis and Wilhelm Stoffel",
year = "2007",
month = "4",
day = "1",
doi = "10.1515/BC.2007.046",
language = "English",
volume = "388",
pages = "405--418",
journal = "Biological chemistry",
issn = "1431-6730",
publisher = "Walter de Gruyter GmbH",
number = "4",

}

RIS

TY - JOUR

T1 - Obesity resistance of the stearoyl-CoA desaturase-deficient (scd1-/-) mouse results from disruption of the epidermal lipid barrier and adaptive thermoregulation

AU - Binczek, Erika

AU - Jenke, Britta

AU - Holz, Barbara

AU - Günter, Robert Heinz

AU - Thevis, Mario

AU - Stoffel, Wilhelm

PY - 2007/4/1

Y1 - 2007/4/1

N2 - Targeted deletion of the stearoyl-CoA desaturase 1 gene (scd1) in mouse causes obesity resistance and a severe skin phenotype. Here, we demonstrate that SCD1 deficiency disrupts the epidermal lipid barrier and leads to uncontrolled transepidermal water loss, breakdown of adaptive thermoregulation and cold resistance, as well as a metabolic wasting syndrome. The loss of omega-hydroxylated very long-chain fatty acids (VLCFA) and ceramides substituted with omega-hydroxylated VLCFA covalently linked to corneocyte surface proteins leads to the disruption of the epidermal lipid barrier in scd1-/- mutants. Artificial occlusion of the skin by topical lipid application largely reconstituted the epidermal barrier and also reversed dysregulation of thermogenesis and cold resistance, as well as the metabolic disturbances. Interestingly, SCD1 deficiency abolished expression of the key transcription factor Lef1, which is essential for interfollicular epidermis, sebaceous glands, and hair follicle development. Finally, the occurrence of SCD1 and a newly described hSCD5 (ACOD4) gene in humans suggests that the scd1-/- mouse mutant might be a valuable animal model for the study of human skin diseases associated with epidermal barrier defects.

AB - Targeted deletion of the stearoyl-CoA desaturase 1 gene (scd1) in mouse causes obesity resistance and a severe skin phenotype. Here, we demonstrate that SCD1 deficiency disrupts the epidermal lipid barrier and leads to uncontrolled transepidermal water loss, breakdown of adaptive thermoregulation and cold resistance, as well as a metabolic wasting syndrome. The loss of omega-hydroxylated very long-chain fatty acids (VLCFA) and ceramides substituted with omega-hydroxylated VLCFA covalently linked to corneocyte surface proteins leads to the disruption of the epidermal lipid barrier in scd1-/- mutants. Artificial occlusion of the skin by topical lipid application largely reconstituted the epidermal barrier and also reversed dysregulation of thermogenesis and cold resistance, as well as the metabolic disturbances. Interestingly, SCD1 deficiency abolished expression of the key transcription factor Lef1, which is essential for interfollicular epidermis, sebaceous glands, and hair follicle development. Finally, the occurrence of SCD1 and a newly described hSCD5 (ACOD4) gene in humans suggests that the scd1-/- mouse mutant might be a valuable animal model for the study of human skin diseases associated with epidermal barrier defects.

KW - Administration, Topical

KW - Animals

KW - Body Temperature Regulation

KW - Ceramides

KW - Cholesterol

KW - Cold Temperature

KW - Down-Regulation

KW - Energy Metabolism

KW - Epidermis

KW - Lipids

KW - Liver

KW - Lymphoid Enhancer-Binding Factor 1

KW - Mice

KW - Mice, Knockout

KW - Obesity

KW - Petrolatum

KW - Signal Transduction

KW - Skin Absorption

KW - Skin Diseases, Genetic

KW - Stearoyl-CoA Desaturase

KW - Transcription Factors

KW - Triglycerides

KW - Wasting Syndrome

KW - Water Loss, Insensible

U2 - 10.1515/BC.2007.046

DO - 10.1515/BC.2007.046

M3 - Journal articles

VL - 388

SP - 405

EP - 418

JO - Biological chemistry

JF - Biological chemistry

SN - 1431-6730

IS - 4

ER -

ID: 133189