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Adiponectin Leptin and Leptin Receptor in Obese Patients with Type 2 Diabetes Treated with Insulin Detemir

机译:胰岛素Detemir治疗肥胖2型糖尿病患者的脂联素瘦素和瘦素受体

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摘要

The aim of the present study is to quantitatively assess the expression of selected regulatory molecules, such as leptin, leptin receptor, and adiponectin in the blood of obese patients with type 2 diabetes both before treatment and after six months of pharmacological therapy with the long-lasting insulin analogue, insulin detemir. A significant decrease in the analysed regulatory molecules, i.e., leptin receptor and adiponectin, was found in blood plasma of the patients with untreated type 2 diabetes. These changes were accompanied by an increase in plasma leptin concentrations. Insulin treatment resulted in the normalization of plasma leptin receptor and adiponectin concentrations. The circulating leptin level did not change following anti-diabetic therapy with insulin detemir. Gender was a significant factor modifying the circulating level of all the analysed regulatory active compounds. Bioinformatic analysis was performed using Matlab with the Signal Processing Toolbox. The conducted discriminant analysis revealed that the leptin receptor, Δw(19), and adiponectin, Δw(21), were the parameters undergoing the most significant quantitative changes during the six-month therapy with insulin detemir. The conducted examinations indicated the contribution of adipocytokines—the biologically-active mediators of systemic metabolism, such as leptin and adiponectin in the pathomechanism of disorders being the basis for obesity which leads to development of insulin resistance, which, in turn, results in the occurrence of type 2 diabetes.
机译:本研究的目的是定量评估肥胖的2型糖尿病患者在治疗前和经过6个月的药物治疗后,血液中所选调节分子(如瘦素,瘦素受体和脂联素)的表达。持久胰岛素类似物,地特胰岛素。在未经治疗的2型糖尿病患者的血浆中发现分析的调节分子,即瘦素受体和脂联素显着降低。这些变化伴随着血浆瘦素浓度的增加。胰岛素治疗导致血浆瘦素受体和脂联素浓度正常化。胰岛素德特米尔抗糖尿病治疗后,循环中的瘦素水平没有变化。性别是影响所有分析的调节活性化合物循环水平的重要因素。使用Matlab和Signal Processing Toolbox进行生物信息学分析。进行的判别分析显示,瘦素受体Δw(19)和脂联素Δw(21)是在六个月的胰岛素detemir治疗期间发生最显着定量变化的参数。进行的检查表明,脂肪细胞因子(系统性代谢的生物活性介质,如瘦素和脂联素)在疾病的发病机理中的作用是肥胖的基础,肥胖导致胰岛素抵抗的发展,继而导致了胰岛素抵抗的发生。 2型糖尿病。

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