Impaired incretin effect is an early sign of glucose dysmetabolism in nondiabetic patients with psoriasis

• Autores: M. Gyldenløve, Lone Skov, Tina Vilsboll, Claus Zachariae, J.J. Holst, K. Knop
• Localización: Journal of Internal Medicine, ISSN-e 1365-2796, Vol. 278, Nº. 6, 2015, págs. 660-670
• Idioma: inglés
• Texto completo no disponible (Saber más ...)
• Resumen

  • Background Patients with psoriasis have an increased risk of type 2 diabetes. The gastrointestinal system plays a major role in normal glucose metabolism, and in healthy individuals, postprandial insulin secretion is largely mediated by the gut incretin hormones. This potentiation is termed the incretin effect and is reduced in type 2 diabetes. The impact of psoriasis on gastrointestinal factors involved in glucose metabolism has not previously been examined.

    Objective To investigate whether the incretin effect, gastrointestinal-mediated glucose disposal (GIGD) and/or secretion of glucagon and gut incretin hormones are impaired in normal glucose-tolerant patients with psoriasis.

    Methods Oral glucose tolerance tests and intravenous isoglycaemic glucose infusions were performed in 12 patients with moderate-to-severe psoriasis and 12 healthy matched control subjects.

    Results In patients with psoriasis, the incretin effect (39% vs. 57%, P = 0.02) and GIGD (53% vs. 61%, P = 0.04) were significantly reduced compared to control subjects. In addition, patients were glucose intolerant and showed exaggerated glucose-dependent insulinotropic polypeptide responses.

    Conclusion These novel findings support the notion that psoriasis is a prediabetic condition and suggest that gastrointestinal-related mechanisms are involved in the increased susceptibility to type 2 diabetes in patients with psoriasis.