Role of Insulin Action in Psoriasis Pathogenesis
The goal of this study is to collect more information from people with plaque psoriasis and to determine if insulin plays a role in the pathogenesis of psoriasis. The main question it aims to answer is if insulin action is preserved or even enhanced in psoriatic lesions despite insulin resistance elsewhere. Participants with plaque psoriasis will have punch biopsies taken of lesional and non-lesional skin after an overnight fast and then during an oral glucose tolerance test. Biopsy specimens will then be assessed for markers of insulin action.
• Body mass index of 25.0-40.0 kg/m2
• Able to understand written and spoken English and/or Spanish
• Written informed consent (in English or Spanish) and any locally required authorization (e.g., Health Insurance Portability and Accountability Act) obtained from the participant prior to performing any protocol-related procedures, including screening evaluations.
• Diagnosed with plaque psoriasis, documented using Psoriasis Area and Severity Index (PASI)
• Glucose metabolism status as follows (determined only retrospectively based on data collected during the study):
‣ For Insulin Sensitive (IS) group:
‣ • Hemoglobin A1c \< 5.7%, and
∙ Fasting plasma glucose \< 95 mg/dL, and
∙ Fasting plasma insulin \< 10 μIU/mL, and
∙ 2-hour post-challenge glucose \< 140 mg/dL
⁃ For Insulin Intermediate (II) group:
‣ • Hemoglobin A1c \< 6.5%, and
‣ • Fasting plasma glucose 80-125 mg/dL, and
‣ • Fasting plasma insulin \< 15 μIU/mL, and
‣ • 2-hour post-challenge glucose \< 200 mg/dL, and
‣ • Not otherwise meeting all criteria for the IS group
⁃ For Insulin Resistant (IR) group:
• Hemoglobin A1c \< 6.5%, and
∙ Fasting plasma glucose 80-125 mg/dL, and
∙ Fasting plasma insulin ≥ 15 μIU/mL, and
∙ 2-hour post-challenge glucose \< 200 mg/dL
⁃ NOTE: Group assignments will be made retroactively, after observational data has been collected. Those not fitting into any of these groups will have their data excluded from further analysis.