Генетика метаболического синдрома: исследования агрегации в семьях

Catedra Medicina de Familie, USMF „Nicolae Testemiţanu”The article is a compilation of research on the heredity qualities of the metabolic syndrome and its components, independent risk factors of cardiovascular diseases and type II diabetes mellitus published in 31 journals over an eleven-year period. There is a general consensus in favor of a strong causative genetic component for metabolic syndrome. This assumes a relatively limited number of loci with pleiotropic effects. Some data supports the hypothesis of intergenetic interaction in the realization of the syndrome. Environmental factors seem to play an important role in the initiation and progression of the metabolic syndrome in individuals with genetic predisposition to the condition/disease.Изучены публикации, посвященные семейному наследованию метаболического синдрома и его составных компонентов, являющихся самостоятельными факторами повышенного риска сердечно-сосудистых заболеваний и сахарного диабета второго типа. Были проанализированы результаты работ по теме с глубиной поиска 11 лет. В частности, были отобраны 31 статья со свободным доступом к полному тексту публикации. Результаты изученных работ свидетельствуют о существовании сильной генетической компоненты в патогенезе метаболического синдрома. Предполагается наличие относительно небольшого количества локусов с плейотропным эффектом в отношении проявлений этого синдрома. Имеются данные в пользу гипотезы межгенного взаимодействия в процессе реализации синдрома. Важная роль в инициации и прогрессировании метаболического синдрома у лиц, предрасположенных к нему генетически, принадлежит факторам внешней среды

Роль макронутриентов при метаболическом синдроме

Catedra Medicina de Familie, USMF „Nicolae Testemiţanu”The objective of the paper was to evaluate publications regarding the role of nutritive substances in induction of pro-inflammatory reactions and oxidative stress in metabolic syndrome. Oxidative stress and pro-inflammatory reactions are characteristic of patients with metabolic syndrome. These can be exacerbated by foods with caloric excess. The degree of the oxidative stress and pro-inflammatory reactions can be substantially reduced by caloric restriction, rational nutrition, and physical activity. Taking into account the high prevalence of the metabolic syndrome and its role in causing cardiovascular and the risk of diabetes mellitus, it is necessary to be expected that physicians to assume proactive tactics in diagnosing individuals with metabolic syndrome and offering them adequate behavioral counseling in the application of programs of non-pharmacological prevention: rational nutrition, a diet of high-quality foods, caloric restriction, micronutrients, and appropriate physical activity.Цель – изучить публикации, касающиеся роли пищевых веществ в индукции воспалительных реакций и оксидативного стресса при метаболическом синдроме. Оксидативный стресс и воспалительные реакции являются характерными для пациентов с метаболическим синдромом. Эти реакции могут быть усилены приемом высококалорийных пищевых продуктов. Степень оксидативного стресса может быть существенно снижена рациональным питанием с ограничением калорийности пищи и физической нагрузкой. Учитывая значительную распространенность метаболического синдрома, его роль в увеличении риска сердечно-сосудистых заболеваний и сахарного диабета второго типа, целесообразной является тактика активного выявления лиц с этим синдромом и адекватное их консультирование по применению немедикаментозных методов профилактики

Asocierea între indicii antropometrici şi parametrii lipidici, la studenţii de la medicină, din Republica Moldova

The 55th National Congress of Cardiology. September 21-24, 2016, Sinaia, România Universitatea de Stat de Medicină şi Farmacie "Nicolae Testemiţanu". Chişină

Single-nucleotide polymorphisms at five loci are associated with C-reactive protein levels in a cohort of Filipino young adults

C-reactive protein (CRP) is a component of non-specific immune defense and is a reliable marker of low-grade inflammation involved in obesity, type 2 diabetes and cardiovascular disease. Genome-wide association studies (GWAS) in middle-aged and elderly populations, predominantly of European descent, demonstrated associations of CRP levels with SNPs at several loci. To examine whether the variants identified are replicated in Filipino young adults, we applied Tobit regression models to study the association of plasma CRP with 12 SNPs at seven loci in a cohort of 1,691 Filipino young adults (aged 21.5 ± 0.3 years) from the Cebu Longitudinal Health and Nutrition Survey (CLHNS). SNPs in or near CRP (P = 3.2 × 10(-11)), HNF1A, IL6R, APOE-APOC1 and LEPR showed significant associations (P < 0.05) and together explained 4.8% of the total variation in CRP. Modest interactions were observed between LEPR rs1892534 and waist circumference (uncorrected P(interaction) = 0.020) and between APOE rs769449 and pathogen exposure (uncorrected P(interaction) = 0.0073) in models predicting CRP. Our results demonstrated that variants in several loci are significantly associated with plasma CRP in Filipino young adults, suggesting shared genetic influences on circulating CRP across populations and age groups

Genetic risk score and adiposity interact to influence triglyceride levels in a cohort of Filipino women

BACKGROUND/OBJECTIVES: Individually, genetic variants only moderately influence cardiometabolic (CM) traits, such as lipid and inflammatory markers. In this study we generated genetic risk scores from a combination of previously reported variants influencing CM traits, and used these scores to explore how adiposity levels could mediate genetic contributions to CM traits. SUBJECTS/METHODS: Participants included 1649 women from the 2005 Cebu Longitudinal Health and Nutrition Survey. Three genetic risk scores were constructed for C-reactive protein (CRP), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TGs). We used linear regression models to assess the association between each genetic risk score and its related trait. We also tested for interactions between each score and measures of adiposity. RESULTS: Each genetic risk score explained a greater proportion of variance in trait levels than any individual genetic variant. We found an interaction between the TG genetic risk score (2.29–14.34 risk alleles) and waist circumference (WC) (P(interaction)=1.66 × 10(−2)). Based on model predictions, for individuals with a higher TG genetic risk score (75th percentile=12), having an elevated WC (⩾80 cm) increased TG levels from 1.32 to 1.71 mmol l(−1). However, for individuals with a lower score (25th percentile=7), having an elevated WC did not significantly change TG levels. CONCLUSIONS: The TG genetic risk score interacted with adiposity to synergistically influence TG levels. For individuals with a genetic predisposition to elevated TG levels, our results suggest that reducing adiposity could possibly prevent further increases in TG levels and thereby lessen the likelihood of adverse health outcomes such as cardiovascular disease