Patients with psoriasis are insulin resistant - 14/03/15
, Heidi Storgaard, PhD b, Jens J. Holst, DMSc c, Tina Vilsbøll, DMSc b, Filip K. Knop, PhD b, c, Lone Skov, PhD, DMSc aAbstract |
Background |
Patients with psoriasis have increased risk of type 2 diabetes. The pathophysiology is largely unknown, but it is hypothesized that systemic inflammation causes insulin resistance. Insulin sensitivity has only been sparsely investigated in patients with psoriasis, and previous studies have used suboptimal methodology. The hyperinsulinemic euglycemic clamp remains the gold standard for quantifying whole-body insulin sensitivity.
Objective |
We sought to investigate if normal glucose-tolerant patients with psoriasis exhibit impaired insulin sensitivity.
Methods |
Three-hour hyperinsulinemic euglycemic clamps were performed in 16 patients with moderate to severe, untreated psoriasis and 16 matched control subjects.
Results |
The 2 groups were similar with regard to age, gender, body mass index, body composition, physical activity, fasting plasma glucose, and glycosylated hemoglobin. Mean ± SEM psoriasis duration was 23 ± 3 years and Psoriasis Area and Severity Index score was 12.7 ± 1.4. Patients with psoriasis exhibited reduced insulin sensitivity compared with control subjects (median M-value 4.5 [range 1.6-14.0] vs 7.4 [range 2.1-10.8] mg/kg/min, P = .046). There were no differences between groups in plasma glucose, insulin, C-peptide, and glucagon during the clamp.
Limitations |
The classic hyperinsulinemic euglycemic clamp technique does not allow assessment of endogenous glucose production.
Conclusion |
Patients with psoriasis were more insulin resistant compared with healthy control subjects. This supports that psoriasis may be a prediabetic condition.
Le texte complet de cet article est disponible en PDF.Key words : hyperinsulinemic euglycemic clamp, insulin resistance/sensitivity, M-value, psoriasis, type 2 diabetes
Abbreviations used : HbA1c, HOMA-IR, tAUC
Plan
| Supported by unrestricted grants from Fonden til Lægevidenskabens Fremme, Kgl. Hofbundtmager Aage Bangs Fond, Psoriasis Forskningsfonden, Robert Wehnert og Kirsten Wehnerts Fond, and Direktør Werner Richter og hustrus legat (n = 1). |
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| Disclosure: Dr Holst received research funding from Novartis (n = 1) and Merck (n = 2); is a member of advisory boards of GlaxoSmithKline, Novo Nordisk, and Zealand Pharmaceuticals; and consulted for Novo Nordisk. Dr Vilsbøll received research funding from Novo Nordisk (n = 3) and Merck (n = 1); Dohme; received lecture fees from or consulted for AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lilly and Company, Merck, Novo Nordisk, Sanofi-Aventis, Takeda, and Zealand Pharma; and is part of the advisory boards of Eli Lilly, Boehringer Ingelheim, Bristol-Myers Squibb/AstraZeneca, Novo Nordisk, Sanofi-Aventis, and Takeda. Dr Knop received research funding from Sanofi-Aventis (n = 2) and lecture fees from AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lilly and Company, Gilead Sciences, Merck, Novo Nordisk, Ono Pharmaceuticals, Sanofi-Aventis, and Zealand Pharma; is part of the advisory boards of Eli Lilly Denmark, Bristol-Myers Squibb/AstraZeneca, Novo Nordisk, Sanofi-Aventis, and Zealand Pharma; and consulted for AstraZeneca, Gilead Sciences, Novo Nordisk, Ono Pharmaceuticals, and Zealand Pharma. Dr Skov received consultancy and/or speaker honoraria from Abbvie, Pfizer, Janssen-Cilag, Merck, and Leo Pharma and is a member of the advisory Boards of Abbvie, Pfizer, Janssen-Cilag, Merck, Eli Lilly, and Novartis. Drs Gyldenløve and Storgaard have no conflicts of interest to declare. |
Vol 72 - N° 4
P. 599-605 - avril 2015 Retour au numéro
Article précédent
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