Tag Archives: type 2 diabetes mellitus
Mitochondrial DNA copy number in leukocytes of patients with type 2 diabetes mellitus and chronic kidney disease
Y. A. Saienko1,2*, D. S. Krasnenkov1, K. K. Midlovets1, V. V. Korcheva1,
Y. E. Rebrova1,3, D. D. Yepishyna1, B. M. Mankovsky1
1SI “D.F. Chebotarev Institute of Gerontology, National Academy
of Medical Sciences of Ukraine”, Kyiv;
2SI “Center for Cardiology and Cardiac Surgery
of the Ministry of Health of Ukraine”, Kyiv
3P.L. Shupyk National University of Health Care of Ukraine, Kyiv;
*e-mail: ysaenko1981@gmail.com
Received: 04 April 2025; Revised: 23 April 2025;
Accepted: 25 April 2025; Available on-line: 12 May 2025
Chronic kidney disease (CKD) as one of the most common complications of type 2 diabetes mellitus (T2DM) significantly increases the risk of cardiovascular disease and mortality. Mitochondrial dysfunction, in particular a reduction in mitochondrial DNA copy number (mtDNA-CN), plays an important role in the development of diabetic complications, including nephropathy. The aim of this study was to determine the mtDNA-CN in peripheral blood leukocytes of patients with T2DM depending on the presence of CKD. A total of 109 individuals were examined, including 20 healthy controls and 89 patients with T2DM divided into groups based on the presence or absence of CKD. The mtDNA-CN in leukocytes was determined using quantitative real-time PCR. Biochemical markers of T2DM and CKD were evaluated, non-parametric tests and correlation analysis were performed. No statistically significant differences in mtDNA-CN level were observed between patients with T2DM and CKD, patients with T2DM without CKD, and the control group (P > 0.05). No associations between mtDNA-CN and kidney function parameters were identified. The absence of mtDNA-CN alterations is assumed to contribute to the relatively satisfactory glycemic control in diabetic groups.
Edaravone reduces the markers of oxidative stress and neuroinflammation in neocortex of rats with acute intracerebral hemorrhage and type 2 diabetes mellitus
V. L. Holubiev*, A. E. Lievykh, V. A. Tkachenko,
Yu. V. Kharchenko, V. I. Zhyliuk
Department of Pharmacology, Dnipro State Medical University, Dnipro, Ukraine;
*e-mail: 209@dmu.edu.ua
Received: 05 August 2024; Revised: 22 October 2024;
Accepted: 21 November 2024; Available on-line: 17 December 2024
Type 2 diabetes mellitus (T2DM) is associated with a higher incidence of hemorrhagic stroke in a severe form. The aim of this study was to estimate the markers of oxidative stress and neuroinflammation in the brain of rats with acute intracerebral hemorrhage (ICH) and T2DM after treatment with edaravone. T2DM was induced by a single intraperitoneal injection of nicotinamide/streptozotocin, ICH – by stereotactic microinjection of bacterial collagenase. Rats were randomized into four groups: 1 – intact control; 2 – T2DM; 3 – T2DM+ICH; 4 – T2DM+ICH+edaravone 6 mg/kg/day. Edaravone (a drug to treat neural injury after acute cerebral ischemic stroke) was administered intraperitoneally for 10 days starting from the 60th day after diabetes mellitus induction and 30 min after ICH induction. Brain homogenates were assessed for the content of advanced glycation end products (AGEs) and advanced oxidation protein products (AOPPs). The levels of TNF-α and 8-hydroxy-2′-deoxyguanosine (8-OHdG) were measured with ELISA. The increased content of 8-OHdG and TNF-α in brain homogenates of animals of T2DM group compared to the control was shown. It was revealed that in brain homogenates of animals of T2DM+ICH group the content of these markers significantly exceeds that for T2DM group, and in addition, an elevated AOPPs level was observed. Our results demonstrated that edaravone prevented the elevation of TNF-α level, reduced oxidative DNA damage by decreasing 8-OHdG content, and attenuated the formation of AGEs and AOPPs in the brains of experimental animals. These findings suggest that edaravone may have therapeutic potential in diabetic patients with acute ICH.
Potential of isothiocyanate sulforaphane from broccoli to combat obesity and type 2 diabetes: involvement of NRF2 regulatory pathway
M. V. Ivanochko1, M. M. Bayliak1, V. I. Lushchak1,2*
1Department of Biochemistry and Biotechnology,
Vasyl Stefanyk Precarpathian National University, Ivano-Frankivsk, Ukraine;
2Research and Development University, Ivano-Frankivsk, Ukraine;
*e-mail: volodymyr.lushchak@pnu.edu.ua
Received: 03 September 2024; Revised: 11 November 2024;
Accepted: 21 November 2024; Available on-line: 17 December 2024
Biologically active food components are now considered to be remedies for the prevention and treatment of metabolic disorders of different etiology. The aim of this review was to analyze the current data on the application of isothiocyanate sulforaphane, found in broccoli and other cruciferous plants, for the treatment of T2DM, obesity, and their comorbidities with the presentation of established molecular, particularly dependent on NF-E2-related factor-2 (Nrf2), and signaling mechanisms of therapeutic effects.
Myonectin, irisin, apelin-13 and Elabela hormones levels as biomarkers for type 2 diabetes mellitus : a systematic review
Abdullah A. H. Al-Rubaye1*, Walaa E. Jasim2, Ahmed A. H. Mohsin2
1Department of Medical Laboratory Technology, College of Health
and Medical Technology, Southern Technical University, Basra, Iraq;
2Department of Medical Laboratory Technology, College of Health
and Medical Technology, Middle Technical University, Baghdad, Iraq;
*e-mail: abdulla.abbas@stu.edu.iq
Received: 16 May 2024; Revised: 23 June 2024;
Accepted: 25 July 2024; Available on-line: 04 September 2024
Insulin resistance is thought to be a key pathophysiologic indicator underlying type 2 diabetes mellitus. Nevertheless, its pathophysiology is complex and remains uncertain. Myokines such as myonectin and irisin produced by muscle tissue were shown to impact the sensitivity to insulin and could play an essential role in the etiology of insulin resistance. Apelin and Elabela are endogenous peptide ligands of the angiotensin II protein J receptor (APJ) that are actively involved in the control of lipid and glucose metabolism, implying a vital role in the management of metabolic conditions like type 2 diabetes. In this review, the data on the level of myonectin, irisin, apelin-13 and Elabela in patients with type 2 diabetes mellitus were analyzed.
The levels of visfatin and toll-like receptors in arterial hypertension and type 2 diabetes mellitus
N. Pokrovska1, S. Mahiiovych1, I. Fomenko2,
L. Biletska2, H. Sklyarova3, L. Kobylinska2*
1Department of Therapy No 1, Medical Diagnostics and Hematology and Transfusion
of FPGE, Danylo Halytsky Lviv National Medical University, Lviv, Ukraine;
2Department of Biochemistry, Danylo Halytsky Lviv National Medical University, Lviv, Ukraine;
3Department of Family Medicine FPGE, Danylo Halytsky Lviv National Medical University, Lviv, Ukraine;
*e-mail: lesyaivanivna.biochemistry@gmail.com
Received: 28 January 2024; Revised: 26 February 2024;
Accepted: 27 February 2024; Available on-line: 30 April 2024
Hypertension and type 2 diabetes mellitus (DM) remain widespread diseases that are becoming more prevalent. The role of visfatin and toll-like receptor (TLR) molecules in the pathogenesis of these diseases requires further research. Our aim was to study changes in visfatin and TLR levels in patients with hypertension and type 2 diabetes. Fifty-one patients were examined and divided into two groups: group 1 included 27 patients with hypertension and group 2 included 24 people with hypertension and type 2 DM. The control group included 18 practically healthy people. All individuals underwent general blood test, coagulogram, biochemical blood test, enzyme immunoassay to determine the level of visfatin and TLR in the blood serum and echocardiography. Hypertrophy of the walls of the left ventricle (LV) was observed in patients of two observed groups. The most common type of LV geometry was concentric hypertrophy (41.2%). The level of visfatin was significantly higher in patients of group 1, while in patients of group 2 it was decreased (P ˂ 0.05) and the level of TLR was increased (P ˂ 0.05). The elevated level of TLR in the serum of patients with hypertension can be considered a factor of low-grade inflammation, especially in combination with type 2 DM. The increase in the concentration of visfatin in hypertension serves as a more sensitive marker compared to TLR regarding the risk of developing comorbid cardiovascular pathology. The therapeutic treatments of patients with type 2 DM cause a reduction in the concentration of visfatin induced by hypertension.
Oxydative stress in type 2 diabetic patients: involvement of HIF-1 alpha AND mTOR genes expression
Y. A. Saenko1, O. O. Gonchar2*, I. M. Mankovska2,
T. I. Drevytska2, L. V. Bratus2, B. M. Mankovsky1,3
1SI “The Scientific and Practical Medical Center of Pediatric Cardiology and Cardiac Surgery
of the Ministry of Health of Ukraine”, Clinic for Adults, Kyiv;
2Department of Hypoxia, Bogomoletz Institute of Physiology,
National Academy of Sciences of Ukraine, Kyiv;
3Shupyk National Healthcare University of Ukraine, Kyiv;
*e-mail:olga.gonchar@i.ua
Received: 22 March 2023; Revised: 25 May 2023;
Accepted: 05 June 2023; Available on-line: 20 June 2023
Biochemical and genetic mechanisms of oxidative stress (OS) developing in the blood of patients with type 2 Diabetes mellitus (T2DM) were studied. Twenty patients with T2DM and 10 healthy persons participated in this study. Lipid peroxidation, the content of protein carbonyls and H2O2 production were measured in blood plasma and erythrocytes as OS biomarkers. Activity of SOD, catalase, and GPx as well as reduced glutathionе (GSH) level in plasma and erythrocytes were estimated. The gene expression of key regulators of oxygen and metabolic homeostasis (HIF-1α and mTOR) in leukocytes were studied. It was found a significant rise in TBARS and protein carbonyls content in plasma as well as H2O2 production in erythrocytes from patients with T2DM compared to control. The diabetic patients also demonstrated an increase in the SOD and catalase activity in plasma and significantly lower GSH content and GPx activity in erythrocytes compared to the healthy participants. The established marked inhibition of mTOR gene expression and the tendency to an increase in HIF-1α gene expression in leukocytes of patients with T2DM may serve as a protective mechanism which counteracts OS developing and oxidative cell damage.
Immunological mechanisms of increased susceptibility to COVID-19 disease and its severe course in patients with diabetes mellitus type 2 and obesity
K. P. Zak1, M. D. Tronko1, S. V. Komisarenko2*
1V. P. Komisarenko Institute of Endocrinology and Metabolism,
National Academy of Medical Sciences of Ukraine, Kyiv;
2Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
*e-mail: svk@biochem.kiev.ua
Received: 28 April 2023; Revised: 28 May 2023;
Accepted: 05 June 2023; Available on-line: 20 June 2023
In this review, we analyze and summarize literature data and the results of our own research related to the immunity status of patients with type 2 diabetes mellitus (T2D) and those T2D patients who were infected with the SARS-CoV-2 virus. It was shown that in the blood plasma of T2D patients, especially those with elevated BMI, the level and ultrastructure of the main cellular components of natural immunity – neutrophils and monocytes – were affected accompanied by high levels of proinflammatory cytokines (IL-1β, IL-6, IL-17 and TNF-α). It was suggested that the increased susceptibility of T2D patients to SARS-CoV-2 infection is primarily due to a weakening of the innate immune defense against pathogens, whereas in T2D patients who have COVID-19, adaptive T-cell immunity disorders accompanied by a cytokine storm prevail. It was concluded that hyperinflammation in T2D+COVID19 patients is the result of enhancement of already existing before SARS-CoV-2 infection T2D-caused disorders of innate and adaptive immunity, in the mechanism of which cytokines and chemokines play a significant role.
Glucose deprivation-induced glycogen degradation and viability are altered in peripheral blood mononuclear cells of type 2 diabetes patients
K. S. Praveen Kumar1, P. Kamarthy2, S. Balakrishna1*
1Department of Cell Biology and Molecular Genetics, Sri Devaraj Urs Academy of Higher Education, Kolar, India;
2Department of General Medicine, Sri Devaraj Urs Medical College, Tamaka, Kolar, India;
*e-mail: sharath@sduu.ac.in
Received: 07 September 2021; Accepted: 21 January 2022
The glycogen pathway plays an important role in glucose homeostasis. Impairment of the glycogen pathway has been linked to diabetes mellitus. The aim of the study is to compare the levels of glucose deprivation-induced glycogen degradation and cell viability in peripheral blood mononuclear cells from type 2 diabetes mellitus patients and healthy controls. This was a case-control study comprising 45 T2DM patients and 45 healthy controls. PBMCs were prepared from peripheral blood by density gradient centrifugation. Glycogen levels were measured by the periodic acid-schiff (PAS) staining method. Glycogen degradation was measured as percent change in PAS-stained cells before and after glucose deprivation. PBMC viability was measured by trypan-blue assay. The levels of glucose deprivation-induced glycogen degradation were 55.4% (IQR: 50.6–61.3) in the T2DM group and 70.5% (IQR: 63.9–72.2) in the healthy control group. The difference between the two groups was statistically significant (P = 0.001). The levels of glucose deprivation-induced cell viability were 70.9% (IQR: 66.3–77.1) in the T2DM group and 87.8% (IQR: 83.7–90.7) in the healthy control group. The difference between the two groups was statistically significant (P = 0.001). Together these results indicate that the glucose deprivation-induced glycogen degradation and viability are reduced in PBMCs of T2DM patients.
The effect of quercetin on oxidative stress markers and mitochondrial permeability transition in the heart of rats with type 2 diabetes
N. I. Gorbenko1, O. Yu. Borikov2, O. V. Ivanova1, E. V. Taran1,
Т. S. Litvinova1, T. V. Kiprych1, A. S. Shalamai3
1V. Danilevsky Institute of Endocrine Pathology Problems, National Academy of Medical Sciences of Ukraine, Kharkiv;
2V. N. Karazin Kharkiv National University, Ukraine;
3PJSC SIC “Borshchahivskiy Chemical-Pharmaceutical Plant”, Kyiv, Ukraine;
е-mail: Gorbenkonat58@ukr.net
Received: 24 June 2019; Accepted: 13 August 2019
Increasing evidence suggests that oxidative stress and induction of mitochondrial permeability transition in cardiomyocytes are linked to tissue damage and the development of diabetic cardiovascular complications. The aim of this study was to assess the effects of quercetin (Q) on oxidative stress and mitochondrial permeability transition in the heart of rats with type 2 diabetes mellitus (DM). Type 2 DM was induced in 12-week-old male Wistar rats by intraperitoneal injections of 25 mg/kg streptozotocin twice per week followed by a high-fat diet during four weeks. The rats were divided into three groups: control intact group (C, n = 8), untreated diabetic group (Diabetes, n = 8) and diabetic rats treated with Q (50 mg/kg/day per os for 8 weeks) after diabetes induction (Diabetes+Q, n = 8). Administration of Q increased insulin sensitivity and normalized the functional state of cardiac mitochondria due to increased aconitase and succinate dehydrogenase activities in rats with type 2 DM. Q also ameliorated oxidative stress, decreasing the level of advanced oxidation protein products and increasing the activity of thioredoxin-reductase in heart mitochondria of diabetic rats. In addition, Ca2+-induced opening of the mitochondrial permeability transition pore was significantly inhibited in diabetic rats treated with Q in comparison with the untreated diabetic group. These data demonstrate that Q can protect against oxidative stress, mitochondrial permeability transition induction and mitochondrial dysfunction in cardiomyocytes of diabetic rats. We suggest that the use of Q may contribute to the amelioration of cardiovascular risk in type 2 DM.