Role of PPARs and their isoforms in metabolic disorders related to insulin resistance and diabetes

COVID-19: Mechanisms, risk factors, genetics, non-coding RNAs and neurologic impairments

“…It plays an important role in fatty acid oxidation processes. The PPARβ/δ is an important mediator of insulin sensitivity [ 83 ] and is directly related to the process of obesity and myocardial hypertrophy through inhibition of nuclear factor kappa B (NF-kB). In vivo and in vitro studies have shown the critical role of the receptor in the regulation of adipocyte differentiation and lipid accumulation in adipose tissue in maintenance of the viability and normal function of differentiated adipocytes.…”

Distribution of Polymorphic Marker of Genes of the Renin-angiotensin System RAS (AGT, AGTR1, АСЕ), ITGB3, PPARG) in Pa-tients With Essential Arterial Hypertension Depending on the Nature of the Nocturnal De-crease of BP

“…Further, we analyzed the frequency of polymorphic markers of the AGTR1 rs5186 and PPARG rs18001282 genes. The minor allele C of the AGTR1 rs5186 gene and the major allele C (Pro12Pro) of the PPARG rs18001282 gene are considered in the literature as risk factors for the development of insulin resistance [4,5,6]. At the same time, the mechanisms of their implementation are different.…”

“…It is the increased activity of RAS proteins in carriers of polymorphic markers of RAS genes that ensures the stabilization of elevated blood pressure at hypertension and provides a pathogenetic link with tissue effects. In this regard, the study of the frequency characteristics of genotypes in the presence of polymorphic gene variants is aimed at identifying candidate genes that increase the risk of developing EAH and its specific clinical forms-occurring with and without a nocturnal decrease of BP [4,5,6,7,8]. The selection of polymorphic markers of the AGTR1 and PPARG genes was aimed at clarifying the role of the genetic component in the formation of nocturnal insulin resistance…”

“…According to the literature, the absence of a nocturnal decrease of BP is associated with the realization of vascular dysfunction against the background of a vegetative imbalance in the form of sympathicotonia and a decrease in the characteristic nocturnal period of increasing the tone of the parasympathetic nervous system [7]. Taking into account the pathogenetic links of increased activity of RAS proteins with activation of the sympathetic link of the nervous system, observed both at the central level (sodium-dependent mechanisms) and at the peripheral level (increased release of norepinephrine in sympathetic terminals) [8], the study of the frequency of occurrence of RAS gene polymorphisms (ACE, AGT, AGTR1) in a group of patients with hypertension without nocturnal decrease in BP (group 1) and with nocturnal decrease in BP (group 2), in combination with the study of the frequency of genotypes of the gene ITGB3(whose polymorphic marker, A2, increases the risk of vascular catastrophes [9]) and the PPARG gene responsible for the formation of insulin resistance [5] (allele C (Pro12Pro)) in patients with metabolic syndrome.…”

The relationship between SNPS in the genes of TLR signal transduction pathway downstream elements and rheumatoid arthritis susceptibility

“…These two transmission ways can be achieved by the cascading of Janus kinase/signal transducer and activator of transcription and mitogen-activated protein kinase (MARK). IL-6/IL-6R/gp130 complex crosslink with JAK in cytoplasm, and promotes the conveying of Acute Phase Reactants (APA), and finally leads to the over-breed of inflammation cells and the damage of natural autoantibody [34][35][36].…”