A long-standing hyperglycaemic condition impairs skin barrier by accelerating skin ageing process.
Uncontrolled chronic hyperglycaemia including type 2 diabetes mellitus (DM) induces many skin problems related to chronic impaired skin barrier state. However, little is known about the skin barrier state of chronic hyperglycaemia patients, the dysfunction of which may be a major cause of their skin problems. In this study, we investigated whether a long-standing hyperglycaemic condition including type 2 DM impairs skin barrier homoeostasis in proportion to the duration and its pathomechanism. We utilized the Otsuka Long-Evans Tokushima Fatty (OLETF) rats as an animal model of long-standing hyperglycaemia and Long-Evans Tokushima Otsuka rats as a control strain. We confirmed that a long-standing hyperglycaemia delayed skin barrier homoeostasis, which correlated with haemoglobin A1c levels. OLETF rats as a long-standing hyperglycaemia model exhibited decreased epidermal lipid synthesis and antimicrobial peptide expression with increasing age. Decreased epidermal lipid synthesis accounted for decreased lamellar body production. In addition, OLETF rats had significantly higher serum levels of advanced glycation end products (AGEs) and elevated levels of the receptor for AGE in the epidermis. A long-standing hyperglycaemic condition impairs skin barrier function including permeability and antimicrobial barriers by accelerating skin ageing process in proportion to the duration of hyperglycaemia, which could be a major pathophysiology underlying cutaneous complications of DM.
Department of Dermatology, Yonsei University Wonju College of Medicine, Wonju, Korea.
Hwa-Young
HY
Park
Jae-Hong
JH
Kim
Minyoung
M
Jung
Choon Hee
CH
Chung
Rosnani
R
Hasham
Chang Seo
CS
Park
Eung Ho
EH
Choi
D000818:Animals; D023181:Antimicrobial Cationic Peptides; D001835:Body Weight; D054804:Cathelicidins / Q000235:genetics; D002454:Cell Differentiation / Q000502:physiology; D049109:Cell Proliferation; D020405:Dermis / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications; D004817:Epidermis / Q000378:metabolism / Q000473:pathology; D015870:Gene Expression / Q000235:genetics; D018149:Glucose Intolerance / Q000097:blood / Q000209:etiology; D005951:Glucose Tolerance Test; D006442:Glycated Hemoglobin / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000097:blood; D006943:Hyperglycemia / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D015603:Keratinocytes / Q000166:cytology / Q000378:metabolism; D008055:Lipids / Q000096:biosynthesis; D010539:Permeability; D051381:Rats; D020334:Rats, Inbred OLETF; D020318:Rats, Long-Evans; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000378:metabolism; D015595:Skin Aging / Q000473:pathology / Q000502:physiology*; D012879:Skin Physiological Phenomena; D014867:Water / Q000378:metabolism; D023083:beta-Defensins / Q000235:genetics
D023181:Antimicrobial Cationic Peptides; D054804:Cathelicidins; D006442:Glycated Hemoglobin; D017127:Glycation End Products, Advanced; D007328:Insulin; D008055:Lipids; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D014867:Water; D023083:beta-Defensins; C549474:beta-defensin-2, rat