Evaluation of serum levels of Irisin as a marker of endothelial dysfunction in patients with type 2 diabetes mellitus

Abstract

Introduction Insulin resistance and obesity have been associated with irisin, a protein in fat cells. The levels of irisin in patients with type 2 diabetes mellitus (T2DM) were significantly lower than those in non‐diabetics. This study aimed to examine the relationship between serum irisin levels and endothelial dysfunction in patients with T2DM. Methods There were 90 participants in this study. We matched 65 patients with T2DM with 25 healthy control participants. A series of tests were performed on the participants, including fasting blood glucose, 2 hours postprandial blood glucose, glycated haemoglobin, triglycerides (TG), total cholesterol, high‐density lipoprotein cholesterol (HDL‐C), low‐density lipoprotein cholesterol (LDL‐C), TG/HDL‐C ratio and albumin/creatinine ratio. In addition to measuring high‐sensitivity C‐reactive protein (hs‐CRP). Enzyme‐linked immunosorbent assay (ELISA) technique was used for estimating irisin concentrations. Results Flow‐mediated dilation (FMD) was significantly lower in patients with T2DM; however, there was a non‐statistically significant difference between healthy controls and patients with T2DM regarding serum Irisin level. CRP and LDL levels were inversely correlated with circulating irisin levels. In a stepwise regression analysis, only the hs‐CRP and LDL were statistically significant in predicting irisin level. Conclusions In patients with T2DM, serum levels of irisin were inversely correlated with hyperglycaemia, body mass index and per cent body fat; this suggests that detecting irisin levels early can prevent cardiovascular diseases from progressing. According to the study results, serum irisin serves as a predictive marker for early cardiovascular disease, thus preventing the disease from progressing. There is a need for further research in order to understand how irisin contributes to the development of atherosclerosis and the development of diabetic complications.

The Association of Adipokines and Myokines in the Blood of Obese Children and Adolescents with Lipoprotein Lipase rs328 Gene Variants

“…Tus, high leptin level promotes lipid catabolism and inhibits lipogenesis [18], and increased apelin lowers lipotoxicity and provides cardio-and neuroprotectivity together with activation of adipocytes proliferation and angiogenesis [19][20][21][22]. In its turn, upregulated irisin limits the energy imbalance in the body, decreases insulin resistance by increasing tissue sensitivity to insulin, promotes β-cell proliferation in the islets of Langerhans, prevents cardiovascular disease progression, inhibits the production of proinfammatory cytokines by adipose tissue, acts as a messenger of metabolic communication between the tissues, and so on [23][24][25][26][27]. In addition, the decreased asprosin level together with leptin predetermines the anorexigenic efect.…”

Diabetes Mellitus Should Be Considered While Analysing Sarcopenia-Related Biomarkers

“…Nevertheless, we must underline that studies with the opposite results involved much fewer participants (73 diabetic individuals with 55 controls and 104 T2DM subjects with 124 controls, respectively). Decreased irisin concentrations in T2DM patients are observed in parallel with cardiovascular complications [131][132][133]. They may have some predictive value in heart failure diagnosis [134,135] and be linked to nephropathy [136].…”

The content of adipokines and myokines in the blood of children and adolescents with different genotypes according to the polymorphism rs662 of the paraoxonase-1 gene

“…Так, повышение уровня лептина играет важное значение в усилении катаболизма липидов и ограничении липогенеза в жировой ткани [18], рост содержания апелина -приводит к снижению липотоксичности и возникновению кардиопротективного и нейропротективного действия [14,15], а увеличение уровня ирисина ограничивает нарушение энергетического баланса в организме при ожирении, увеличивает чувствительность тканей к инсулину, снижая тем самым инсулинорезистентность, способствует пролиферации β-клеток островков Лангерганса, предупреждает прогрессирование сердечно-сосудистых заболеваний, тормозит продукцию провоспалительных цитокинов жировой тканью, выступает в роли медиатора коммуникации метаболизма между различными тканями организма и др. [19][20][21][22]. Вместе с тем следует особо заметить, что данный миокин секретируется не только клетками мышечной, но и жировой ткани [19,23].…”