Basic and clinical science posters: Cell signalling, endocrinology and metabolism

Basic and clinical science posters: Cell signalling, endocrinology and metabolism P54 The skin: A novel regulator of whole‐body glucose homeostasisE EVANS1, X Kodji2, S Sayers1, Y Xia1, S Brain2, M Philpott3, R Hannen3, P Caton11Department of Diabetes, King's College London, London, UK, 2Vascular Biology Department, King's College London, London, UK, 3Centre for Cell Biology & Cutaneous Research, Queen Mary University of London, London, UKAims: The inflammatory skin disease psoriasis is an independent risk factor for development of insulin resistance and Type 2 diabetes, and the presence of psoriasis is a strong predictor of Type 2 diabetes progression and severity. We used the well‐established imiquimod (IMQ) mouse model of psoriasis to investigate the effects of skin inflammation on insulin sensitivity and beta cell function.Methods: Mice were topically administered 75‐mg Aldara cream (Meda Pharma; 3.75‐mg IMQ/day) or Vaseline control to a shaved dorsal region for four consecutive days (n = 5 to 8). On day five, mice were fasted for glucose tolerance testing or killed in the fed state with blood and tissues collected for analysis (qPCR, enzyme‐linked immunoabsorbent assay and immunofluorescence).Results: IMQ induced a psoriatic‐like phenotype in mouse skin, evidenced by thickening, erythema and inflammation of the skin. IMQ induced elevated pro‐inflammatory cytokine gene expression (interleukin (IL)‐1beta 7.91 ± 1.85; IL6 2.50 ± 0.49, IL17 1.42 ± 0.27) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Diabetic Medicine Wiley

Basic and clinical science posters: Cell signalling, endocrinology and metabolism

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Publisher
Wiley Subscription Services, Inc., A Wiley Company
Copyright
Diabetic Medicine © 2018 Diabetes UK
ISSN
0742-3071
eISSN
1464-5491
D.O.I.
10.1111/dme.6_13571
Publisher site
See Article on Publisher Site

Abstract

P54 The skin: A novel regulator of whole‐body glucose homeostasisE EVANS1, X Kodji2, S Sayers1, Y Xia1, S Brain2, M Philpott3, R Hannen3, P Caton11Department of Diabetes, King's College London, London, UK, 2Vascular Biology Department, King's College London, London, UK, 3Centre for Cell Biology & Cutaneous Research, Queen Mary University of London, London, UKAims: The inflammatory skin disease psoriasis is an independent risk factor for development of insulin resistance and Type 2 diabetes, and the presence of psoriasis is a strong predictor of Type 2 diabetes progression and severity. We used the well‐established imiquimod (IMQ) mouse model of psoriasis to investigate the effects of skin inflammation on insulin sensitivity and beta cell function.Methods: Mice were topically administered 75‐mg Aldara cream (Meda Pharma; 3.75‐mg IMQ/day) or Vaseline control to a shaved dorsal region for four consecutive days (n = 5 to 8). On day five, mice were fasted for glucose tolerance testing or killed in the fed state with blood and tissues collected for analysis (qPCR, enzyme‐linked immunoabsorbent assay and immunofluorescence).Results: IMQ induced a psoriatic‐like phenotype in mouse skin, evidenced by thickening, erythema and inflammation of the skin. IMQ induced elevated pro‐inflammatory cytokine gene expression (interleukin (IL)‐1beta 7.91 ± 1.85; IL6 2.50 ± 0.49, IL17 1.42 ± 0.27)

Journal

Diabetic MedicineWiley

Published: Jan 1, 2018

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