De-regulation of diabetic regulatory genes in psoriasis: Deciphering the unsolved riddle

• Our study highlights the genes involved in the pathogenesis of Ps-T2D.
• We identified three biomarkers for T2D in Ps patients (GSK3B, PTPN1 and STX4).
• ACE showed suggestive association with Ps.
• We hypothesize that Ps and T2D share common causative gene/polygenes.

The purpose of our study was to identify the currently lacking molecular mechanism that accounts for the co-occurrence of two seemingly disparate diseases: psoriasis and type II diabetes. We aimed to investigate a panel of 84 genes related to the diabetic regulatory network in psoriasis (Ps), psoriasis type II diabetes (Ps-T2D), type II diabetes (T2D) and healthy control (HC). We hypothesize that such attempts would provide novel diagnostic markers and/or insights into pathogenesis of the disease. A quantitative Real Time-PCR Human Diabetes RT2 Profiler PCR Array was chosen to explore the expression profile 84 diabetic genes in study subjects. Statistical analysis was carried out using appropriate software. The analysis revealed three candidate genes GSK3B, PTPN1, STX4 that are differentially expressed in study subjects. GSK3B was highly significant in Ps-T2D (P = 0.00018, FR = − 26.6), followed by Ps (P = 0.0028, FR = − 14.5) and T2D groups (P = 0.032, FR = − 5.9). PTPN1 showed significant association only with PS-T2D (P = 0.00027, FR = − 8.5). STX4 showed significant association with both Ps (P = 0.0002, FR = − 20) and Ps-T2D (P = 0.0016, FR = − 11.2). ACE represents an additional marker that showed suggestive association with Ps (P = 0.0079, FR = − 9.37). Our study highlights the complex genetics of Ps-T2D and present biomarkers for the development of T2D in Ps cases.