Interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1) and diabetes mellitus type 2

Interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1) and diabetes mellitus type 2

Celkové hodnotenie

Vedecká práca
80%
Prevedenie (dizajn)
60%
Diskusná interakcia
20%
PoužívateľVedecká prácaDizajnDiskusná interakcia
PharmDr. Stanislava Jankyová PhD.100%60%-
Ing. Zuzana Brnoliaková PhD.60%60%20%
ISBN: 978-80-970712-6-4

Interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1) and diabetes mellitus type 2

Jana Kalninová1 , Vladimír Jakuš
1 Comenius University, Faculty of Medicine, Institute of Medical Chemistry, Biochemistry and Clinical Biochemistry, Sasinkova 2, 811 08 Bratislava, Slovakia
jana.kalninova@fmed.uniba.sk

Diabetes mellitus is a metabolic disorder which is characterized by hyperglycemia and glucose intolerance due to insulin deficiency, impaired effectiveness of insulin action or, both. Diabetes mellitus, especially type 2 diabetes mellitus (T2DM), is a public health problem which has reached epidemic proportions due the rapidly increasing rates of this disease worldwide. Activation of inflammatory processes may contribute to the development of T2DM. Inflammation appears to be a major mechanism responsible for vascular damage leading to the clinically well-recognized complications of diabetes. Inflammation is considered to be a key regulator of the pathogenesis of T2DM, but what triggers this inflammation is still unknown. The aim of our study was to evaluate impact of glycemic control on inflammation (IL-8, MCP-1) in patients with T2DM.

Plasma were obtained from  23 healthy control subjects and 69 patients with T2DM. T2DM patients were divided into 2 groups according the value of glycated hemoglobin (HbA1c). The patients with HbA1c < or = 6 % had good glycemic control (GGC group, n=37) and those with HbA1c > 6% had poor glycemic control (PGC group, n=32) regardless of presence of diabetic complications. Plasma levels of IL-8 and MCP-1 were determined using Fluorokine MAP cytokine multiplex kit designed for use with Athena Multi-Lyte Luminex® 100™ analyser produced at R&D Systems (Minneapolis, MN, USA).

Our results showed that plasma levels of IL-8 and MCP-1 were significantly increased in PGC and GGC groups, the levels were higher in PGC group in comparison with GGC group, but the difference was not significant. In control group  were found significantly negative correlation of IL-6 and IL-8 with DBP (r= -0.470, p=0.027, respectively r= -0.707, p<0.0001). In PGC group were significantly negative correlation between IL-8 and albumin (r= -0.793, p=0.033) and significantly positive correlation between IL-8 and MCP-1 (r=0.624, p=0.0001). In GGC group we found significantly positive correlation between IL-8 and MCP-1 (r=0.584, p=0.004). In control group we found significantly negative correlation between IL-8 and LDL (r= -0.489, p=0.046) and between IL-8 and MCP-1 (r=0.768, p=0.002). We observed the effect of treatment in patients who used oral OAD agents (n=16), OAD agents and were on a diet (n=7), also in patients who were treated with combination insulin and OAD agents (n=5) and patients who were treated with insulin alone (n=6). We observed beneficial impact of treatment with oral antidiabetic (OAD) agents and OAD agents + insulin on levels of IL-8 in comparison with treatment with insulin alone.

The obtained results showed that monitoring of parameters of low-grade inflammation especially in patients with poor glycemic control may be useful to recognize the risk of diabetic complications. Despite of good glycemic compensation of patients with T2DM remained significantly elevated levels of inflammatory markers in comparison with healthy controls. There were beneficial impact of treatment with OAD agents, resp. with OAD agents + insulin in lowering of low-grade inflammation.

Poďakovanie: 

This study was supported by the grants VEGA 1-0375-09 and VEGA 1-0451-12.

Zdroje: 
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Diskusia

Dobry den, vasa praca si kladla za ulohu zistit vyznam glykemickej kontroly vo vztahu IL-1 a MCP-1, avsak ci bola kontrola lepsia ci horsia vysledky to neovplyvnilo. Mohli by ste oddiskutovat tento vysledok? Preco ani v pripade dobrej glykemickej kompenzacie uvedene parametre nepoklesli, existuju podla vas na to nejake fyziologicke vysvetlenia? Dakujem za odpoved. ZB