Cardiovascular risk factors aggregate in determined individuals. Patients with Type 2 diabetes mellitus (T2DM) have higher cardiovascular This study aimed to investigate insulinresistance (IR) and β-cell function using the homeostasis model assessment (HOMA) indexes in a general Kazakh population and determine the effect he effect that cardiovascular factors may have on those indexes. We conducted a cross-sectional study among employees of the Khoja Akhmet Yassawi International Kazakh-Turkish University (Turkistan, Kazakhstan) aged between 27 and 69 years. Sociodemographic variables, anthropometric measurements (body mass, height, waist circumference, hip circumference), and blood pressure were obtained. Fasting blood samples were collected to measure insulin, glucose, total cholesterol (TC), triglycerides (TG), and high- (HDL) andlow-density lipoprotein (LDL) levels. Oral glucose tolerance tests were performed. Hierarchical and K-means cluster analyses were obtained. The final sample was composed of 427 participants. Spearmen correlation analysis showed that cardiovascular parameters were statistically associated with HOMA-β (p < 0.001) and not with HOMA IR. Participants were aggregated into the three clusters where the cluster with a higher age and cardiovascular risk revealed deficient β-cell functioning, but not IR (p < 0.000 and p = 0.982). Common and easy to obtain biochemical and anthropometric measurements capturing relevant cardiovascular risk factors have been demonstrated to be associated with significant deficiency in insulin secretion. Although further longitudinal studies of the incidence of T2DM are needed, this study highlights that cardiovascular profiling has a significant role not just for risk stratification of patients for cardiovascular prevention but also for targeted vigilant glucose monitoring.

Background and Objectives: Metabolic syndrome is a common condition associated with a higher risk of diabetes and cardiovascular disease. Altered iron metabolism, especially iron overload, may play a role in the development of insulin resistance, hypertension, and other metabolic abnormalities. Although the p.C282Y polymorphism of the HFE gene affects iron regulation and may contribute to these metabolic changes, previous studies have reported inconsistent findings, thus highlighting the need for a comprehensive meta-analysis. Materials and Methods: A systematic literature search was performed in PubMed, Scopus, and Web of Science to examine the associations between the HFE p.C282Y polymorphism and components of metabolic syndrome. Observational studies were included if they compared the frequencies of diabetes, hypertension, and abdominal obesity, as well as levels of triglycerides and high-density lipoprotein cholesterol, between carriers and non-carriers of the p.C282Y variant. Results: A total of 17 studies were included in the meta-analysis, and the pooled analysis demonstrated no significant association between the HFE p.C282Y polymorphism and diabetes, hypertension, triglyceride levels, or HDL cholesterol levels under the codominant model. Similarly, analyses performed using the homozygous model did not reveal any statistically significant associations. Conclusions: This meta-analysis found no statistically significant association between the HFE p.C282Y polymorphism and any of the considered components of metabolic syndrome under the examined genetic models.

Iron metabolism has long been linked to metabolic syndrome (MetS), but it is still unclear at which step—iron sensing, hepcidin regulation, export, transport, or storage—genetic variation matters the most. There are almost no studies on iron metabolism genes in Kazakhs in particular. Using whole-exome sequencing (WES) data from 96 Kazakh adults (52 with MetS), we examined 18 SNPs across six iron metabolism genes—HFE, SLC40A1, TMPRSS6, FTL, TFR2, and TF. Associations with iron biomarkers and MS components were tested by linear regression adjusted for age, sex, and BMI, with FDR correction, haplotype analysis, and bootstrap mediation analysis. Significant effects clustered at two distinct steps of iron metabolism: hepcidin regulation (TMPRSS6) and iron transport (TF). The T allele of TF rs12769 raised serum transferrin (β = +0.32 g/L; p_FDR = 0.002) while lowering both TSAT (β = −4.25%) and ferritin (β = −0.36 log-units); haplotype analysis confirmed rs12769 as the driver. The TMPRSS6 C–G–C haplotype was associated with lower fasting glucose (β = −1.19 mmol/L; p = 0.023), and TF rs12769 emerged as a robust FDR-significant determinant of serum transferrin (p_FDR = 0.002). Bootstrap mediation analysis (5000 iterations) showed that the TMPRSS6 effect on glucose is not mediated by ferritin, serum iron, transferrin, TSAT, or sTfR (all ACME p > 0.20), while Total and Direct Effects remained robust (p ≤ 0.054). In Kazakhs, iron-metabolism genes appear to influence fasting glucose through direct mechanisms not captured by the standard iron biomarker panel; alternative pathways involving hepatic enzymes, hepcidin, or inflammation warrant investigation in larger cohorts.

Relevance. Metabolic syndrome is a cluster of interconnected metabolic abnormalities characterized by central obesity, hypertension, dyslipidemia, and impaired glucose metabolism. One important but under-studied factor influencing the development and severity of metabolic syndrome is mineral metabolism, including calcium, magnesium, and phosphorus levels. An imbalance of these minerals can disrupt insulin sensitivity, promote inflammatory processes, and affect lipid and carbohydrate metabolism. Objective. To summarize and critically evaluate current evidence on the relationship between mineral metabolism (calcium, magnesium, phosphorus, parathyroid hormone, and vitamin D) and the clinical and metabolic manifestations of metabolic syndrome in adults. Materials and methods. A structured literature search was conducted in PubMed, Scopus, and Google Scholar. The review primarily included studies published between January 2018 and March 2026, while earlier landmark publications were included when necessary to provide physiological background. Нәтижелері. Әдебиеттерді талдау минералдық алмасу бұзылыстарының метаболизмдік синдромның дамуы және оның клиникалық-метаболикалық көріністерімен тығыз байланысты екенін көрсетті. Ең сенімді деректер магний тапшылығына, сондай-ақ кальций, фосфор, паратиреоидты гормон және D витамині алмасуының бұзылыстарына қатысты алынды, олар инсулинге төзімділікпен және басқа да метаболикалық бұзылыстармен байланысты болды. Conclusions. The literature review confirms that mineral metabolism disorders, including serum calcium, magnesium, and phosphorus levels, are closely related to the clinical and metabolic manifestations of metabolic syndrome.

Background: Insulin resistance (IR) is a major pathogenic factor in metabolic syndrome and related diseases. It is challenging to accurately measure IR due to high cost and technical complexity. TyG-derived indices have been proposed as simple and reliable surrogates for assessing insulin resistance. The present study aimed to investigate the association between TyG-derived indices and indicators of mineral metabolism and bone quality and to examine sex-specific differences. Methods: This cross-sectional study included 330 adults aged 18–65 years. Age-adjusted partial correlation analyses and multivariable linear regression models were performed to examine the associations between TyG indices and several metabolic parameters, minerals, and QUS bone indices. Results: TyG–BMI was strongly correlated with triglycerides (females: r = 0.51; males: r = 0.54, both p < 0.001), glucose (females: r = 0.54, p < 0.001), and hip circumference (females: r = 0.77; males: r = 0.58, both p < 0.001). HDL showed inverse associations (females: r = −0.41, p < 0.001). In females, TyG–BMI demonstrated modest positive correlations with bone parameters, including BQI (r = 0.21, p = 0.002), T-score and Z-score (r = 0.21, p = 0.002 for both), SOS (r = 0.19, p = 0.007), and BUA (r = 0.18, p = 0.010), whereas no significant associations were observed in males. In multivariable models, TyG–BMI in females remained independently associated with glucose (β = 9.77, p < 0.001), waist circumference (β = 2.94, p < 0.001), and HDL (β = −26.6, p < 0.001), but not with mineral or bone parameters. Conclusions: The TyG-derived indices, most notably TyG–BMI, are useful indicators of metabolic status that correlate with bone quality yet exhibit sex-specific associations. These findings support the role of TyG-derived indices as accessible surrogate markers of metabolic status and demonstrate sex-specific associations with bone quality parameters.

Introduction. Recently, melatonin and its agonists have been proven to be effective in the treatment of jet lag syndrome, insomnia, stress, fear, anger, anxiety, stress conditions, which are accompanied by sleep disorders, increase the immune system of the whole body, and as antioxidant protection. Melatonin is known to be an important chronobiological molecule that exerts its effect on any system in the body. The role and pharmacological effect of melatonin in the gastrointestinal system is still one of the important topics, and research continues in various directions. Aim. To monitor the therapeutic effects of melatonin in relation to ethanol concentration in an ethanol-induced experimental gastric ulcer model. Material’s and method. A prospective preclinical (experimental) single-center study. The work was carried out using laboratory rats. The research work was carried out for each of the 6 groups, in a model of gastric ulcer induced by ethanol of various concentrations (100-75-60%) and melatonin was administered to the ulcer (15 mg/kg) and the control group. The obtained data were subjected to statistical analysis using a trial version of the SPSS statistical program (SPSS 20 Inc, Chicago, IL, USA), the critical significance level (p) was assumed to be 0.05. Results. In addition to this increase in the wound area, melatonin administered as a prophylactic subcutaneous injection reduced the overall wound area. In the group of wounds induced by ethanol (100%), the wound area was 15.01±1.92 mm, after intraperitoneal injection of melatonin (15 mg/kg), and after 30 minutes the wound area was 14.01±1.74 mm in the 100% ethanol-induced group and 13. 24±1.71 mm, in the 75% ethanol-induced group, 11.87±1.45 mm in the melatonin + 75% ethanol-induced group, 11.52±1.15 mm in the 60% ethanol-induced group and 6.12± 0.54 mm in the melatonin + 60% ethanol-induced group. Conclusion. In this study, melatonin showed a positive effect in the prevention and treatment of ethanol-induced ulcers at different concentrations. A significant change was observed at higher levels of melatonin inhibition of ethanol exposure at lower concentrations. Актуальность. В последнее время мелатонин и его агонисты доказали свою эффективность в качестве антиоксидантной защиты при лечении синдрома смены биологических ритмов, бессонницы, стресса, страха, гнева, тревоги, стрессовых состояний, которые сопровождаются нарушениями сна и повышают иммунитет всего организма. Известно, что мелатонин является важной хронобиологической молекулой, оказывающей влияние на любую систему организма. Роль и фармакологический эффект мелатонина в системе желудочно-кишечного тракта до сих пор остается одной из важных тем и исследования продолжаются в различных направлениях. Цель. Исследование терапевтических эффектов мелатонина в зависимости от концентрации этанола в модели экспериментальной язвы желудка. Материалы и методы. Проспективное доклиническое (экспериментальное) одноцентровое исследование. Работа проводилась с использованием лабораторных крыс. Исследовательская работа проводилась для каждой из 6 груп, в модели язвы желудка, индуцированной этанолом различной концентраций (100-75-60%) и вводился мелатонин до язвы (15 мг/кг) и контрольной группе. Полученные данные были подвергнуты статистическому анализу с помощью пробной версии статистической программы SPSS (SPSS 20 Inc, Chicago, IL, USA), критический уровень значимости (р) принимался за 0,05. Результаты. В желудке крыс этанол при макроскопическом анализе в зависимости от концентрации увеличивал площадь раны. Мелатонин вводимый в виде профилактической подкожной инъекции, уменьшал общую площадь раны. В группе индуцированным этанолом (100%), площадь раны без введения мелатонина составила 15,01±1,92 мм., а с введением мелатонина (15 мг/кг) до язвы площадь раны уменшилась на 14,01±1,74 мм., и в группе 75% этанола, площадь раны без введения мелатонина составила 13,24±1,71 мм., введением мелатонина до язвы площадь раны уменшилась на 11,87±1,45 мм., и в группе 60% этанола, площадь раны без введения мелатонина составила 11,52±1,15 мм., и введением мелатонина до язвы площадь раны уменшилась на 6,12 ± 0,54 мм. Выводы. В этом исследовании мелатонин показал положительный эффект в профилактике и лечении язв, вызванных этанолом, в...