BACKGROUND: According to the International Diabetes Federation (IDF) in 2021, one in ten adults worldwide suffers from diabetes, of which 90% have type 2 diabetes (T2D). Numerous studies indicate that blood PUFA levels affect lipid metabolism. Blood PUFA levels are affected not only by their dietary intake, but also by their metabolism by desaturase enzymes encoded by the fatty acid desaturase 1 (FADS1) and fatty acid desaturase 2 (FADS2) genes.

AIM: To study the contribution of the FADS1, FADS2 genes to the risk of developing type 2 diabetes mellitus among the Yakut population.

MATERIALS AND METHODS: A total of 541 volunteers, ethnic Yakuts up to the third generation, participated in the study. The sample of patients with type 2 diabetes mellitus consisted of 95 patients from the endocrinology department of the Republican Hospital No. 2 of the State Budgetary Institution “Emergency Medical Care Center”. The comparison group was a sample of 446 volunteers without chronic diseases. A group of healthy Yakuts was divided into subgroups based on body mass index (BMI). Single nucleotide polymorphisms were determined by polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP) analysis.

RESULTS: The present study established a high frequency of ancestral alleles for SNP rs174537 (72.8 - 78.1%), for SNP rs174546 (71.3–78.1%) and for the deletion rs3834458 (72.8–77.5%) in Yakut populations. Analysis of the strength of the association of alleles and genotypes of the FADS1 / FASD2 genes with type 2 diabetes did not show statistically significant values. Analysis of pairwise linkage disequilibrium and assessment of haplotypes for the studied polymorphisms was r²=0.93-1.00. An association of the TTT haplotype with type 2 diabetes mellitus, which was 14.5 times more common in patients, was revealed.

CONCLUSION: The results of this study may provide input for future nutrition and diet research to examine the effects of dietary PUFA exposure on the epigenetic regulation of PUFA biosynthesis and metabolism. Further work is needed to elucidate the specific mechanisms by which the FADS gene cluster and diet influence LC PUFA levels in humans and how they influence inflammation and disease.

BACKGROUND: The effect of glucagon on metabolic processes is ambiguous: on the one hand, an excess of this hormone in the postprandial period increases glycemia, on the other hand, it can contribute to weight loss. In this regard, it is important to assess the secretion of the natural glucagon/glucagon-like peptide-1 coagonist oxyntomodulin in obese individuals with or without type 2 diabetes (T2D).

AIM: To investigate the secretion levels of GLP-1, glucagon, and the GLP-1/glucagon coagonist oxyntomodulin in patients with obesity, with or without T2D, during the weight loss process after bariatric surgery.

MATERIALS AND METHODS: The study involved participants with morbid obesity, with or without T2D, all of whom underwent bariatric surgery. Prior to the procedure, and then at 3 and 6 months post-surgery, the patients participated in hyperinsulinemic euglycemic clamp tests and OGTT. During these assessments, glucose, glucagon, GLP-1, and oxyntomodulin levels were measured at 0, 30, and 120 minutes.

RESULTS: The research included 44 obese patients without T2D and 42 with T2D. Baseline characteristics, including age, height, weight, BMI, waist circumference, and hip circumference, did not show significant differences between the two groups. Patients without T2D showed a lower degree of insulin resistance, a lower glucagon level, and greater preservation of GLP-1 secretion. Additionally, these patients initially exhibited higher levels of oxyntomodulin compared to those with T2D (area under the curve 2.08 [1.61; 2.50] ng/ml*h vs 1.64 [1.07; 1.78] ng/ml*h , p<0.00005). Following weight loss, oxyntomodulin secretion levels rose in both groups (in the T2DM (-) group: 2.35 [1.9; 3.28] ng/ml*h at 3 months, 2.55 [2.02; 3.35] ng/ml*h at 6 months, p<0.00001; in the T2DM (+) group: 2.27 [1.95; 2.61] ng/ml*h at 3 months; 2.4 [1.99; 2.72] ng/ml*h at  6 months, p<0.00001) with no significant intergroup differences at 3 and 6 months after ­surgery.

CONCLUSION: Baseline oxyntomodulin levels were significantly higher in patients with normal carbohydrate metabolism than in patients with type 2 diabetes and increased equally in both groups at 3 and 6 months after bariatric intervention. These results may indicate potential protective functions of oxyntomodulin, but further studies are needed.

BACKGROUND: Women with type 1 diabetes mellitus (DM) have a high frequency of menstrual irregularities and perinatal complications. New methods for monitoring the glycemic profile provide opportunities to analyze the effectiveness of insulin therapy regimens in maintaining the reproductive health of these patients.

AIM: The aim of the study was to assess the relationship between glycemic profile patterns, pro- and antioxidant statuses, and ovarian reserve parameters in type 1 DM patients.

MATERIALS AND METHODS: This study included 60 type 1 DM women, of whom 30 patients aged 33.0 [30.0; 35.0] years used the multiple insulin injections (MII) regimen (Group 1). In this group, patients were divided into two subgroups: not exceeding the percentage of hyperglycemia above the target range for more than 35% of the day (Group 1A) and exceeding this range (Group 1B). The continuous subcutaneous insulin infusion (CSII) regimen was administered to other 30 patients (Group 2). They were subdivided identically into Groups 2A and 2B. We analyzed continuous glucose monitoring data using the FreeStyle Libre Flash Glucose Monitoring System and evaluated blood malonic dialdehyde level, catalase activity and 3-nitrotyrosine level, as well as ovarian volume, antral follicle count, anti-Müllerian hormone and follicle-stimulating hormone levels.

RESULTS: We found no differences in the time in range in Groups 1A and 2A. The HbA1c level was higher in the time above range group of women using MII. Blood 3-nitrotyrosine level in Group 1B was 161.4 [110.6; 232.1] nmol/l and differed from that in Group 2B (42.4 [19.1; 64.9] nmol/l; p<0.01). A relationship was found between catalase activity and soluble receptor for advanced glycation end-products (sRAGE) levels in Group 2A (rs=0.857; p<0.05). The antral follicle count tended to increase when the target range of glucose levels was exceeded above 7.8 mmol/l for more than 35% of the day.

CONCLUSION: Preliminary data were obtained on the relationship between hyperglycemia exceeding 7.8 mmol/l for more than 35% of the day with oxidative stress parameters, sRAGE levels, and a tendency towards an increase in the antral follicle count in women with type 1 DM.

BACKGROUND. Patients with diabetic chronic kidney disease (CKD) stage 5 comprise the most severe group of dialysis patients. The half-life of this group from the moment of starting renal replacement therapy is between 3.5 and 5 years. Transplantation treatment is the preferred method for treating this category of patients.

AIM. The objective of the study was to methodically examine the preliminary and long-term outcomes of transplantation treatment in patients diagnosed with type 1 diabetes mellitus (DM1) and stage 4–5 chronic kidney disease.

MATERIALS AND METHODS. From 2007 to 2023, the kidney and pancreas transplant unit performed 146 kidney transplantations and 84 simultaneous pancreas-kidney transplantations (SPKT) in patients with CKD as an outcome of DM1.

RESULTS. During the entire follow-up period, the overall survival rate for kidney transplant patients was 67.1% (n=98) and 59.6% (n=87) for renal grafts; among SPKT patients, these rates were 76.2% (n=64) and 70.2% (n=59), respectively, with a pancreas graft survival rate of 64.3% (n=54).

CONCLUSION. The results of transplant treatment of patients with DM1 and stage 4-5 CKD are presented in this article.

BACKGROUND: One of the common and unfavorable complications in patients with long-term diabetes mellitus (DM) is diabetic foot syndrome (DFS). The type of pathogen plays a key role in the course of the infectious process, its severity, the nature of tissue damage, the rate of spread and the outcome of the disease. Improving the rationality and efficacy of antibiotic therapy (ABT) in patients with SDS infection is currently an important practical task, both to improve patient outcomes and to prevent the spread of antibiotic resistance (ABR).

AIM: To study the species diversity and ABR profile of etiologic agents of lower extremity infections in patients with SDS.

MATERIALS AND METHODS: Retrospective descriptive clinical and epidemiologic study. The analysis of 83 cases of hospitalization of patients with SDS in City Clinical Hospital №3 named after B.I.Alperovich (Tomsk) in 2023–2024 was carried out. 118 isolates — microorganisms identified in patients from wound discharge were studied.

RESULTS: The structure of pathogens was represented by Gram-negative (67,8%), Gram-positive (29,7%) flora and fungi (2,5%). In the species structure, the predominant role belonged to S. aureus (20,3 %), K. pneumoniae (17,8%), P. aeruginosa (13,6%), E. coli (8,5%) and P. mirabilis (8,5%). K. pneumoniae lost sensitivity to ampicillin and significantly decreased sensitivity to amoxicillin/clavulanic acid. The frequency of ABR of K. pneumoniae and E. coli to fluoroquinolones was often higher than to drugs from the group of cephalosporins. At the same time, pathogens demonstrated good sensitivity to carbapenems and aminoglycosides. The ABR of S. aureus strains to erythromycin was 25,0%, 12,5% of isolates were insensitive to oxacillin.

CONCLUSION: Gram-negative etiologic agents are characterized by an unfavorable sensitivity profile mainly to cephalosporins and fluoroquinolones. The etiologic share of MRSA accounts for 12,5% of SDS-associated infections. The data obtained have important clinical significance in the optimization of empirical ABT of infections in diabetic foot patients.

BACKGROUND/OBJECTIVES: Diabetes risk screening tools are essential for identifying individuals with prediabetes and preventing the progression to diabetes. However, systematic reviews focusing on such tools, particularly for prediabetes screening, are scarce. This scoping review examines the characteristics, development methods, and effectiveness of diabetes risk assessment tools in identifying prediabetes and predicting its progression to diabetes.

MATERIALS AND METHODS: A scoping review was conducted following the Joanna Briggs Institute methodology. Searches were performed in PubMed, ScienceDirect, and Google Scholar, complemented by citation tracking. Eligible studies included asymptomatic adults with prediabetes. Studies were excluded if they lacked relevant data, were not in English, or had no validation measures. Data were extracted independently by two reviewers and synthesized narratively, focusing on study design, risk model features, performance statistics, and quality assessments.

RESULTS: Fourteen studies met the inclusion criteria, covering 26 risk models. Sensitivity and specificity were used in 9 risk screening tools, with Hazard Ratios and C-Statistics assessing diabetes progression in six. Common risk factors included age, BMI, family history of diabetes, and hypertension. Non-invasive tools and predictive models showed promise, with most studies assessed as having a low risk of bias using QUADAS-2. High-sensitivity tools utilizing FBG, HbA1c, and OGTT cutoffs demonstrated effectiveness but require balancing cost and feasibility for broader implementation.

CONCLUSION: A range of different screening tools has been tested that could identify people with prediabetes or a high risk of developing type 2 diabetes. However, where sufficient evidence was available to compare tools across studies the performance of these tools was inconsistent. Several tools have only been investigated in single studies, with uncertainty around their wider generalisability. Clinicians or researchers wishing to screen people for prediabetes or a high risk of developing type 2 diabetes using any of these tools should be aware of their potential limitations.

The full text of the article is available in the electronic version of the journal on the website www.dia-endojournals.ru

BACKGROUND: Type 2 diabetes mellitus (T2DM) is associated with oxidative stress, leading to insulin resistance. Thiosulfate sulfurtransferase (TST) is mitochondrial enzyme involved in the reaction with cyanide, endogenous hydrogen sulfide (H₂S), and reactive oxygen species.

AIM: This study aimed to investigate the relationship between TST enzyme and both oxidative and anti-oxidative stress markers in T2DM patients. TST is believed to be related to oxidative stress, which plays a crucial role in determining the severity and progression of the disease.

MATERIALS AND METHODS: A case-control study included (150) T2DM patients who were taking the drug Metformin (Glucophage) 500 mg twice daily as well as (150) healthy subjects aged between 33 to 65 years. TST activity was estimated based on the sulfur transfer and thiocyanate formation. Malonaldehyde (MDA), peroxynitrite, peroxidase, aryl esterase, vitamin C, vitamin E, thioredoxin (Trx) and glutathione (GSH) were also measured. In addition to clinical markers, all measurements were made in two replicates, statistical analyses were conducted, and data were presented as a median and interquartile range.

RESULTS: TST activity was significantly lower (by 55%) in T2DM patients compared to the controls (8.5 (3.8) vs. 19 (2) U/ml, respectively). There was an inverse relationship between enzyme activity and age, whereas enzyme activity increased with smoking. Antioxidant compounds such as vitamin C, vitamin E, GSH, Trx, and arylesterase activity were significantly lower, while oxidant markers including peroxidase activity, MDA, and peroxynitrite, were significantly higher. TST activity showed a negative correlation with MDA and peroxynitrite, and a positive correlation with Trx and GSH.

CONCLUSION: TST activity is reduced in T2DM patients and is associated with oxidative stress. This suggest that TST may play a protective role against oxidative stress, making it a potential indicator of metabolic regulation and a possible therapeutic target.

Most processes in the human body and other living organisms are governed by biorhythms. The term biorhythms refers to periodically recurring changes in biological processes. Biological rhythms are genetically fixed and are crucial factors in natural selection and adaptation of organisms. In humans, circadian rhythms are regulated by central and peripheral clocks. The central clock is located in the suprachiasmatic nucleus (SCN) of the anterior hypothalamus, while peripheral clocks are found in various tissues and organs of the human body, including the brain, pancreas, liver, adipose tissue, gastrointestinal tract, and muscles. External and internal signals are in constant synchronization, ensuring homeostasis. A mismatch between internal biological clocks and external signals can lead to desynchronization of circadian rhythms. Desynchronization of the circadian rhythm may result in the onset of metabolically associated diseases, including the development of type 2 diabetes, obesity, and poorer glycemic control. This article examines the impact of circadian rhythms on biological processes and hormone secretion, as well as the relationship between circadian rhythms and glucose metabolism in individuals with type 2 diabetes and normoglycemia.

This literature review is the first in a series of articles devoted to the mutual influence of diabetes mellitus (DM) and hemostatic disorders associated with endothelial dysfunction (ED), changes in platelet activity, plasma-coagulation link of hemostasis, activity of natural anticoagulants and fibrinolysis. The main mechanisms of development of ED, the possibilities of its detection not only in scientific research, but also in routine clinical practice are analyzed. The main principles of both non-drug and drug correction of ED are also given. Emphasis is placed on the possibility of using for this purpose drugs with and without a hypoglycemic effect. An opinion is expressed about the presence of a reverse effect of ED on the imbalance of carbohydrate metabolism, which, in the opinion of the authors, can significantly expand the understanding of the role of these disorders not only in the development of complications, but also in the pathogenesis of diabetes mellitus itself.

It is known that in diabetes mellitus (DM), cardiac pathology can develop not only as a result of damage to the coronary arteries. No less significant is the role of non-coronary myocardial dysfunction, including that associated with chronic hyperglycemia. In 2024, a consensus document was published, developed by experts from the Heart Failure (HF) Association of the European Society of Cardiology (ESC) and the Working Group on Myocardial and Pericardial Diseases of the ESC, in which the term «diabetic myocardial disorder» was proposed for the first time. This condition is defined as systolic and/or diastolic myocardial dysfunction in DM and develops under the combined influence of several factors, with hyperglycemia playing the leading role. The concept of «diabetic cardiomyopathy» (DCM) has been actively used by scientists for a long time, but to date it has not been implemented at the level of complications of DM by analogy with diabetic nephropathy and is not included in the spectrum of diseases classified as diabetic macroangiopathy. Pathological processes characteristic of DCM and HF with preserved ejection fraction (HFpEF) in DM are similar, and therefore these conditions are often equated. The diagnostic concept of HFpEF is being improved. According to modern concepts, patients with type 2 DM (DM2) and asymptomatic structural and/or functional myocardial abnormalities are diagnosed with subclinical HF. The importance of timely recognition of this stage is that current treatment options for DM2 make it possible to stop or slow down its progression to symptomatic HF. This article discusses current views on the etiopathogenesis of DCM in patients with DM, summarizes recommendations on the diagnostic capabilities of diastolic myocardial dysfunction, subclinical HF and HFpEF, and emphasizes the importance of timely assessment of the risk of developing clinically manifest HF in patients with DM2.

Obesity in patients with type 1 diabetes (T1D) is an increasingly important problem in diabetology. According to recent studies, the prevalence of overweight and obesity among patients with T1D varies from 15 to 50%. About a quarter of patients with T1D have metabolic syndrome. On the one hand, weight gain in patients with T1D reflects a general population trend. On the other hand, diabetes-related factors such as basal-bolus insulin therapy, chronic insulin overdose, hypoglycemia, and psychological problems associated with the disease can be promoters of weight gain. The relationship between T1D and obesity can be bidirectional. It has been established that overweight and obesity increase the risk of T1D, probably contributing to the autoimmune destruction of beta cells. Individuals with overweight and obesity, compared with patients with normal body weight, more often have insulin resistance, dyslipidemia and require higher doses of insulin to achieve targets of glycemic control. Obesity in individuals with T1D a risk factor for diabetic microvascular complications, arterial hypertension, chronic kidney disease, chronic heart failure, cardiovascular events, non-alcoholic fatty liver disease, and is associated with increased mortality. Therefore, maintaining normal body weight should be considered as an important option in the management of T1D. Education, moderate calorie restriction diet, and physical activity are the basis of the strategy for the prevention and treatment of obesity in individuals with T1D. Glucagon-like peptide-1 agonists, dual agonists of glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide, sodium-glucose cotransporter 2 inhibitors, and metformin are considered promising therapeutic options; however, data on the efficacy and safety of these drugs in patients with T1D are still limited. Experience in performing bariatric interventions in individuals with T1D and morbid obesity is accumulating. Further research is needed to create programs for the prevention and treatment of obesity in patients with T1D.

The current focus of type 2 diabetes mellitus (T2DM) control has shifted from HbA1c to glycemic variability (GV) due to its key role in the accelerated development of diabetic complications, in addition to chronic hyperglycemia. The central link in the early stage of dysglycemia is β-cell dysfunction with subsequent loss of their mass with an important role of hyperglucagonemia at all stages of the diabetic continuum. Coordinated work of α and β-cells with the help of two endogenous incretins: glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) is of decisive importance for maintaining glucose homeostasis. The ability of dipeptidyl peptidase-4 (DPP-4) inhibitors to not only maintain β-cell mass and promote insulin release, but also simultaneously correct glucagon secretion from α-cells, preventing hypoglycemia, by preserving bioactive GLP-1 and GIP intact, attracts special attention to these drugs.

The place of DPP-4 inhibitors among various pharmacological treatment options for T2DM is considered: details of glycemic control and the role in reducing GV with safety in relation to the risk of cardiovascular diseases (CVD) are clarified. New data on the mechanisms of action of dipeptidase-4 are presented, which, as a new adipokine with systemic activity and cellular specificity in the regulation of not only metabolic homeostasis, but also inflammatory processes, may represent a key link between central obesity, insulin resistance (IR) and atherosclerosis. Accordingly, the pathophysiological relationship between T2DM and CVD through IR and low-level inflammation has determined a shift in therapy goals from blood glucose control to general risk factor management, which clarifies the role and place of DPP-4 inhibitors.

The insufficient awareness of the medical community about hereditary lipodystrophies makes it difficult to detect this pathology. Despite progress in understanding the molecular-genetic basis of various lipodystrophy syndromes, many patients still elude the attention of doctors and only learn about their condition at later stages. The American Association of Clinical Endocrinology (AACE) has established an expert working group that includes practicing physicians and leaders in the treatment and research of lipodystrophy syndromes to develop clinical guidelines.

Lipodystrophy syndromes represent a heterogeneous group of extremely rare diseases, all characterized by a deficiency of adipose tissue in the absence of dietary deprivation or a catabolic state. Inherited lipodystrophies are associated with potentially serious metabolic complications, including diabetes, hypertriglyceridemia, hepatic steatosis, polycystic ovary syndrome, and acanthosis nigricans. Lipodystrophy syndromes are heterogeneous and diagnosed based on a combination of phenotypic manifestations, clinical examination data, and supplemented by the results of genetic testing. Patients with a confirmed diagnosis should undergo annual screening for diseases associated with these syndromes in order to detect them earlier. According to the literature, the prevalence of inherited lipodystrophy syndromes is estimated to be 1 case per 1 million people.

Due to their rare occurrence, most clinicians are unfamiliar with this diagnosis and its treatment principles. Therefore, raising awareness among physicians from various specialties about this orphan pathology is crucial for earlier diagnosis, which is the main objective of this publication.