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Войти в исследования Scandinavian journal of rheumatology · 2010
Insulin sensitivity and related cytokines, chemokines, and adipokines in polymyalgia rheumatica.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Kreiner F, Galbo H
Аннотация
OBJECTIVES: To evaluate the insulin sensitivity (IS) and levels of peptides with impact on IS in polymyalgia rheumatica (PMR) before and after prednisolone treatment.
METHODS: Fifteen PMR patients and 15 controls were included. Subjects were studied before and after treatment with prednisolone for 14 days (20 mg/day). Composite IS indices were calculated from glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Plasma concentrations of tumour necrosis factor alpha (TNF), interleukin (IL)-6, IL-8, monocyte chemoattractant protein 1 (MCP-1), resistin, leptin, and adiponectin were measured.
RESULTS: Prednisolone abolished symptoms and increased physical activity within 1–2 days; erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were normalized at day 14. Before treatment, IS was lower in patients vs. controls (p < 0.001). Following treatment, IS was restored in patients (p < 0.01) but not changed in controls (p > 0.05). IL-6, TNF, and IL-8 were higher in patients vs. controls before treatment (p < 0.05–0.001), and decreased after treatment in patients (p < 0.001) but did not change in controls. Before treatment, adiponectin was lower in patients vs. controls (p < 0.05). During treatment, adiponectin increased in both groups (p < 0.05). Leptin did not differ between untreated patients and controls but increased in both groups (p < 0.05). MCP-1 and resistin did not differ (p > 0.05).
CONCLUSION: IS is decreased in PMR, probably reflecting abnormal cytokine and adipokine levels. Treatment with prednisolone improves IS along with normalization of cytokine and adipokine levels and physical activity.
METHODS: Fifteen PMR patients and 15 controls were included. Subjects were studied before and after treatment with prednisolone for 14 days (20 mg/day). Composite IS indices were calculated from glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Plasma concentrations of tumour necrosis factor alpha (TNF), interleukin (IL)-6, IL-8, monocyte chemoattractant protein 1 (MCP-1), resistin, leptin, and adiponectin were measured.
RESULTS: Prednisolone abolished symptoms and increased physical activity within 1–2 days; erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were normalized at day 14. Before treatment, IS was lower in patients vs. controls (p < 0.001). Following treatment, IS was restored in patients (p < 0.01) but not changed in controls (p > 0.05). IL-6, TNF, and IL-8 were higher in patients vs. controls before treatment (p < 0.05–0.001), and decreased after treatment in patients (p < 0.001) but did not change in controls. Before treatment, adiponectin was lower in patients vs. controls (p < 0.05). During treatment, adiponectin increased in both groups (p < 0.05). Leptin did not differ between untreated patients and controls but increased in both groups (p < 0.05). MCP-1 and resistin did not differ (p > 0.05).
CONCLUSION: IS is decreased in PMR, probably reflecting abnormal cytokine and adipokine levels. Treatment with prednisolone improves IS along with normalization of cytokine and adipokine levels and physical activity.