Type I Diabetes Mellitus Suppresses Experimental Skin Carcinogenesis

Author:

Giakoumaki Maria1,Lambrou George I.23ORCID,Vlachodimitropoulos Dimitrios4ORCID,Tagka Anna5,Vitsos Andreas1ORCID,Kyriazi Maria1,Dimakopoulou Aggeliki1,Anagnostou Vasiliki1,Karasmani Marina1,Deli Heleni1,Grigoropoulos Andreas1,Karalis Evangelos1ORCID,Rallis Michail Christou1ORCID,Black Homer S.6

Affiliation:

1. Division of Pharmaceutical Technology, Department of Pharmacy, School of Health Sciences, National and Kapodistrian University of Athens, Panepistimiopolis, 15784 Athens, Greece

2. Choremeio Research Laboratory, First Department of Pediatrics, School of Health Sciences, Medical School, National and Kapodistrian University of Athens, Thivon & Levaeias 8, Goudi, 11527 Athens, Greece

3. Research Institute of Maternal and Child Health & Precision Medicine, National and Kapodistrian University of Athens, Thivon & Levadeias 8, 11527 Athens, Greece

4. Department of Forensic Medicine and Toxicology, Medical School, National and Kapodistrian University of Athens, 75, Mikras Asias Street, 11527 Athens, Greece

5. First Department of Dermatology and Venereology, ‘Andreas Syggros” Hospital, School of Medicine, National and Kapodistrian University of Athens, Ionos Dragoumi 5, 11621 Athens, Greece

6. Department of Dermatology, Baylor College of Medicine, Houston, TX 77030, USA

Abstract

This study explores the previously uncharted territory of the effects of ultraviolet (UV) radiation on diabetic skin, compared to its well-documented impact on normal skin, particularly focusing on carcinogenesis and aging. Employing hairless SKH-hr2, Type 1 and 2 diabetic, and nondiabetic male mice, the research subjected these to UV radiation thrice weekly for eight months. The investigation included comprehensive assessments of photoaging and photocarcinogenesis in diabetic versus normal skin, measuring factors such as hydration, trans-epidermal water loss, elasticity, skin thickness, melanin, sebum content, stratum corneum exfoliation and body weight, alongside photo documentation. Additionally, oxidative stress and the presence of hydrophilic antioxidants (uric acid and glutathione) in the stratum corneum were evaluated. Histopathological examination post-sacrifice provided insights into the morphological changes. Findings reveal that under UV exposure, Type 1 diabetic skin showed heightened dehydration, thinning, and signs of accelerated aging. Remarkably, Type 1 diabetic mice did not develop squamous cell carcinoma or pigmented nevi, contrary to normal and Type 2 diabetic skin. This unexpected resistance to UV-induced skin cancers in Type 1 diabetic skin prompts a crucial need for further research to uncover the underlying mechanisms providing this resistance.

Publisher

MDPI AG

Reference47 articles.

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5. Fitzpatrick, T.B., Eisen, A.Z., and Wolff, K. (1987). Dermatology in General Medicine, McGraw-Hill. [3rd ed.].

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