Metabolic syndrome (MetS), today a major global public health problem, is a cluster of clinical, metabolic, and biochemical abnormalities, such as central adiposity, hypertension, insulin resistance, and dyslipidemias. These MetS-related traits significantly increase the risk of type 2 diabetes mellitus, adverse cardiac events, stroke, and hepatic steatosis. The pathogenesis of MetS is multifactorial, with the interplay of environmental, nutritional, and genetic factors. Chronic low-grade inflammation together with visceral adipose tissue, adipocyte dysfunction, and insulin resistance plays a major role in the progression of the syndrome by impairing lipid and glucose homeostasis in insulin-sensitive tissues, such as the liver, muscle, and adipocytes. Adipose-derived inflammatory cytokines and non-esterified fatty acids establish the link between central obesity IR, inflammation, and atherogenesis. Various studies have reported an association between MetS and related traits with single-nucleotide polymorphisms of different susceptibility genes. Modulation of cytokine levels, pro-oxidants, and disturbed energy homeostasis, in relation to the genetic variations, is described in this review of the recent literature, which also provides updated data regarding the epidemiology, diagnostic criteria, and pathogenesis of MetS.

Aim: To identify genetic variants in promoter areas of IL-6 -174 G>C and TNF-α -308 G>A in metabolic syndrome (Met S) and controls and associate them with Met S and serum cytokine levels.It was a cross-sectional study, including 224 cases of Met S and 200 controls. A fasting blood sample was taken and biochemical parameters including serum glucose, insulin, lipid profile, interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) were measured. Restriction fragment length polymorphism was used to identify the genetic variants of IL-6 and TNF-α. Serum levels of IL-6 and TNF-α and insulin resistance were significantly higher in cases than the controls. IL-6 showed significant positive correlation with HOMA-IR and TNF-α. CC genotype of IL-6 was associated with the increased risk of Met S (P=0.016, OR for CC vs GC+GG = 2.33, CI: 1.15–4.71). There was no significant difference of TNF-α genotypes between the cases and the controls. Serum TNF-α and IL-6 levels were significantly higher in AA and CC genotypes of TNF-α (-308 G>A) and IL-6 (-174 G>C) as compared with the GG (P=0.00 and P=0.001). Significant correlation of IL-6 with TNF-α and insulin resistance was observed that may provide us a therapeutic target for preventing metabolic derangements from insulin resistance.

Preeclampsia (PE) is the leading cause of maternal and fetal morbidity and mortality. It complicates around 2%–10% pregnancies worldwide due to imbalance between proangiogenic and anti-angiogenic factors, leading to incomplete placentation, ischemia, and endothelial dysfunction. The study was aimed to analyze the mRNA expression of vascular endothelial growth factor (VEGF) and its receptors, i.e., VEGF receptor-1 (VEGFR-1), VEGF receptor-2 (VEGFR-2), and soluble Fms-like tyrosine kinase-1 (sFlt-1) from maternal peripheral blood mononuclear cells (PBMCs) of PE patients. This was a cross-sectional comparative study comprising 18 normotensive and 18 PE patients; the patients were further divided as early-onset preeclampsia (EOP) and late-onset preeclampsia (LOP). The expression level of VEGF, its receptors (VEGFR-1 and VEGFR-2), and sFlt-1 was investigated using real-time polymerase chain reaction. There was a significant change in the mRNA expression with a decrease in VEGF, VEGFR-1, and VEGFR-2 and an increase in sFlt-1 in PBMCs of PE and normal pregnancies (P < 0.001). sFlt-1 mRNA expression was increased by 2.95-fold in the PE group with an inverse correlation with expression of VEGFR-2 (Spearman's rho = 0.68). Based on these findings, we conclude that PE is associated with decrease in the mRNA expression of VEGF, VEGFR-1, and VEGFR-2 as compared to an increase in sFlt-1 in PBMCs.

Diabetic Cardiomyopathy (DCM) is characterized by myocardial dysfunction caused by diabetes mellitus. After-effects of diabetic cardiomyopathy are far more lethal than non-diabetic cardiomyopathy. More than 300 million people suffer from diabetes and cardiovascular disorder which is expected to be elevated to an alarming figure of 450 million by 2030. Recent studies suggested that miRNA plays important role in the onset of diabetic cardiomyopathy. This study was designed to identify the miRNA that is responsible for the onset of diabetic cardiomyopathy using in silico and in vitro approaches. In this study, to identify the miRNA responsible for the onset of diabetic cardiomyopathy, in silico analysis was done to predict the role of these circulating miRNAs in type 2 diabetic cardiomyopathy. Shared miRNAs that are present in both diseases were selected for further analysis. Total RNA and miRNA were extracted from blood samples taken from type 2 diabetic patients as well as healthy controls to analyze the expression of important genes like AKT, VEGF, IGF, FGF1, ANGPT2 using Real-time PCR. The expression of ANGPT2 was up-regulated and AKT, VEGF, IGF, FGF1 were down-regulated in DCM patients as compared to healthy controls. The miRNA expression of miR-17 was up-regulated and miR-24, miR-150, miR-199a, miR-214, and miR-320a were down-regulated in the DCM patients as compared to healthy controls. This shows that dysregulation of target genes and miRNA may contribute towards the pathogenesis of DCM and more studies should be conducted to elucidate the role of circulating miRNAs to use them as therapeutic and diagnostic options.

Objective: To measure the peripheral blood mononuclear cells (PBMCs) mRNA expression of placental growth factor (PlGF), Transforming growth factor beta (TGF-), and soluble Endoglin (sEng) in the blood of preeclamptic and normotensive pregnant women.