Endocrine Abstracts (2008) 16 P257

Cytokines secretion in long-standing diabetes mellitus type 1 and 2: associations with low-grae systemic inflammation

Krystallenia I Alexandraki1, Christina Piperi1, Panayiotis D Ziakas2, Nikolaos V Apostolopoulos4, Konstantinos Makrilakis5, Vassiliki Syriou2, Evanthia Diamanti-Kandarakis3, Gregory A Kaltsas2 & Anastasios Kalofoutis1


1Laboratory of Biological Chemistry, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece; 2Division of Endocrinology, Department of Pathophysiology, Laiko University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece; 3Division of Endocrinology, First Department of Medicine, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece; 4Department of Obstretics and Gynaecology, Homerton University Hospital, London, UK; 5Diabetologic Center, First Department of Propaedeutic Medicine, Laiko University Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.


Background: Low-grade systemic chronic inflammation has been recognized in diabetes. The purpose of this study was the assessment of proinflammatory cytokines secretion profile in long-standing diabetes along with the presence of systemic inflammation.

Methods: Twenty patients with type 1 (T1DM: 7 women, age (±S.E.M.): 30.90±1.93 years, duration of disease: 142.47±28.34 months) and 21 patients with type 2 diabetes mellitus T2DM: 11 women, age: 58.67±3.01 years, duration of disease: 68.32±17.36 months) were studied along with 34 healthy subjects (17 women, age: 53.61±2.48 years). Metabolic parameters were assessed. Serum levels of high sensitivity C-reactive protein, interleukin-1β, interleukin-6 and tumor necrosis factor-α were determined by ELISA. The number of cytokine-secreting peripheral blood mononuclear cells before and after mitogenic stimulation was determined by the Enzyme-Linked-Immuno-spot assay.

Results: Patients with T2DM had an adverse metabolic profile compared to patients with T1DM and controls. There was a difference in hsCRP, sIL-6 and TNF-α level between groups, with higher levels being observed in T2DM and lower levels in controls. T2DM patients were characterized by higher count of cytokine-secreting PBMCs compared to patients with T1DM and controls. Patients with T1DM showed a higher count of IL-1β-secreting PBMCs compared to controls. After stimulation with PMA, an increased number of all cytokine-secreting PBMCs were observed in the studied groups, but this rise was higher in the control group compared to diabetic groups.

Conclusion: The present study revealed increased levels of several circulating markers of chronic inflammation in diabetic groups compared to healthy subjects, but the grade of inflammation was higher in T2DM. Furthermore, both groups presented a defect in cytokines production by the PBMCs after stimulation compared to healthy subjects. The presence of low grade inflammation and the abnormal PBMCs function in diabetic patients may result in the long-term sequelae of diabetes such as the accelerated atherosclerotic process and the susceptibility to infections.