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International Journal of Physiology and Pathophysiology

Published 4 issues per year

ISSN Print: 2155-014X

ISSN Online: 2155-0158

SJR: 0.116

The Content of Blood Leptin and Activity of Systemic Inflammatory Response in Patients with Type 2 Diabetes Mellitus depending on Weight and Length of the Process

Volume 6, Issue 3, 2015, pp. 213-219
DOI: 10.1615/IntJPhysPathophys.v6.i3.50
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ABSTRACT

The aim of the study was to establish the relationship between the blood leptin content and the markers of generalized non-specific inflammation in patients with type 2 diabetes mellitus (DM), depending on its duration, excess weight and obesity. We compared the contents of leptin, interleukins (IL) IL-2, IL-6, and tumor necrosis factor α (TNF-α) in groups with different duration of type 2 diabetes mellitus, in normal, overweight, and obese patients. In the patients with high leptin content, significantly lower levels of TNF-α (7.82 ± 0.34 ng / ml) have been found. The positive correlation of the latter with body mass index (r = 0.48, P < 0.0001) and IL-6 (r = 0.13, P = 0.019) was observed, resulting from the increased pool of visceral adipose tissue that produces leptin and 10 − 35% of IL-6. In patients with newly diagnosed type 2 diabetes mellitus, the levels of leptin (19.35 ± 1.39 ng / ml) and TNF-α (7.82 ± 0.94 ng / ml) were significantly lower compared to the control values. The highest contents of leptin and cytokines were observed in the patients with diabetes duration of 5 to 10 years. As a rule, cardiovascular complications are developed just in this period. In the group of patients with normal weight, the contents of leptin (6.39 ± 1.15 ng / ml) were the lowest, whereas the contents of TNF-α (11.37 ± 3.77 ng / ml) and IL-6 (10.12 ± 6.91 ng / ml) were the highest. Perhaps it is the high content of these cytokines that makes it possible to maintain a normal body weight in these patients. It is known that under prolonged glucose - and lipotoxicity metabolic immunosuppression emerges, defined by the changes in T-cell immunity, which also contributes to autoimmunity in type 2.diabetes mellitus.

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