Adipocytokines in metabolically healthy obesity

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Sofia G. Shulkina
Elena N. Smirnova
Maxim I. Yudin
Mikhail A. Osadchuk
Maxim V. Trushin *
(*) Corresponding Author:
Maxim V. Trushin | mtrushin@mail.ru

Abstract

The aim of the investigation was to study the relationship among adipokines, markers of subclinical inflammation and endothelial dysfunction in patients with metabolic healthy obesity (MHO). The study included 50 persons aged 25-50 years with obesity in the absence of metabolic disorders (International Diabetes Federation criteria, 2005, marked as MHO), the control group consisted of 50 healthy respondents without obesity. We studied clinical and biochemical parameters, insulin resistance index (HOMA-IR), levels of leptin, soluble leptin receptors (sLR), resistin, adiponectin, C-reactive protein (CRP-hs), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), endothelin-1 (ET-1), von Willebrand factor, free leptin index was calculated in a formula (FLI = leptin × 100 / sLR). In MHO patients, independently of HOMA-IR index, there was an increase in leptin, FLI, resistin, VEGF, and IL-6 parameters. The concentration of CRP-hs and TNF-α in MHO group with HOMA-IR ≥2.7 was increased. Systolic blood pressure correlated with leptin level (r=0.43, P<0.05), FLI (r=0.54; P=0.01), TNF-α (r=0.44; P<0.05) and IL-6 (r=0.33; P<0.05); diastolic blood pressure - with leptin level (r=0.35, P<0.05). Links between high density lipoproteins and leptin (r=–0.55 and r=–0.60; P<0.01), resistin (r=0.32; P<0.05 and r=0.60; P<0.01) and VEGF (r=–0.70, P<0.01) were established. The VEGF level correlated with HOMA-IR (r=0.62; P<0.01), leptin (r=0.29; P<0.05), FLI (r=0.50; P<0.05), resistin (r=0.70; P<0.01), IL-6 (r=0.74, P<0.01) and ET-1 (r=0.29; P<0.05). Obese patients without metabolic disorders, having normotension and normal insulin sensitivity, are less influenced to adverse cardiovascular risks due to less expressed hormonal and inflammatory activation of adipose tissue and, as a result, less pronounced endothelial dysfunction. While insulin resistance develops, cardiovascular risk increases due to activation of subclinical inflammation, angiogenic endothelial dysfunction and leptin resistance.


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