علي بليغ عبد الرزاق القريشي

Background: Coronary artery disease (CAD) is the global leading cause of mortality, it develops mainly from atherosclerotic changes. Lipoprotein lipase (LPL) is the principal enzyme metabolizing chylomicrons and very low-density lipoprotein, the impairment of its activity increases the possibility of CAD initiation. Methods: One hundred CAD patients and 100 apparently healthy controls were included in this study. Serum lipid concentrations were measured by standard procedures. DNA was extracted and analyzed for the rs320 SNP of LPL gene polymorphism by ARMS-PCR. Aim: To verify the influence of rs320 single nucleotide polymorphism of LPL gene on the occurrence of CAD in a sample of Iraqi persons. Results: Atherogenic serum lipid concentrations were found to elevate significantly in CAD patients in comparison to the control group. Analysis of the genotypes and allele frequencies demonstrated significantly increased number of the heterozygous, TG (OR= 2.9, CI95%= 1.34-6.35, P= 0.006), and homozygous, GG (OR= 11.5, CI95%= 5.27-25.14, P=0.000), genotype carriers in the CAD group with respect to the control group. The minor allele G was significantly (P=0.000) higher in patients when compared to the control groups. The estimation of serum lipid concentrations exhibited significantly higher levels of cholesterol, triglycerides and LDL-C and a lowering of HDL-C concentration concomitant with the GG genotype. Conclusion: LPL gene polymorphism, rs320, increases the risk of CAD by 2.9 and 11.5 folds in Iraqi carriers of the TG and GG genotype respectively. Moreover, the G allele elevates the atherogenic serum lipid concentrations. Keywords: rs320; LPL; coronary artery disease; ARMS

Background: Recently, the polymorphisms of the vitamin D receptor gene has been linked to several autoimmune diseases. The main goal of this study is to explore the association between VDR gene polymorphisms (rs731236, rs2228570, rs1544410, rs7975232) and the risk of Hashimoto’s thyroiditis (HT) among the Iraqi population. Methods: Peripheral blood samples were used to isolate genomic DNAs from 180 HT patients and 200 healthy controls. Four VDR gene loci were amplified, and the obtained amplicons were then digested using the restriction enzymes FokI, BsmI, TaqI and ApaI. The digested fragments were then electrophoresed on agarose gel (2.5%). HT polymorphisms and estimated haplotypes were computed by odds ratios (ORs). Results: After stratification by age, gender and body mass index (BMI), univariate logistic regression statistical analysis showed that there was a significantly higher incidence of FokI (rs2228570) polymorphisms in HT pa tients compared to healthy controls. As compared to the HT patient group, healthy individuals had a significantly higher incidence of TaqI (rs731236) and BsmI (rs1544410) polymorphisms. Linkage disequilibrium (LD) analysis of pairs of SNPs revealed that the polymorphisms in the VDR gene (rs731236 A/G and rs7975232 G/C) were in strong LD in an HT model (D ′ = 0.86). Furthermore, AAGC and AAGT haplotype models (OR = 1.5, 95% CI: 1.1–2.1; OR = 1.61, 95% CI: 1.06–2.45, P = 0.02) were associated with an increased risk of HT, while the AACC haplotype model (OR = 0.37, 95% CI: 0.15 – –0.90, P= 0.02) exhibited a significantly decreased the risk of developing HT. Conclusion: Our research supports the association between HT and the FokI polymorphism among the Iraqi population. Additionally, the haplotype analysis demonstrates that these individuals with positive FokI poly morphism are more susceptible to HT due to a combination of mutant alleles derived from different VDR gene variants.

Background: Diabetic nephropathy (DN) is a major cause of end-stage kidney disease, associated with severe complications. Numerous studies have found connections between variations in the ADIPOQ gene and both type two diabetes mellitus (DM) and DN. Objective: The objective of the present investigation is to evaluate the correlation between the ADIPOQ polymorphism (rs1501299) and the exposed to DN in the Iraqi patients. Materials and Methods: A case-control study involved 121 subjects divided into three groups: 45 type 2 diabetes (T2DM) patients with nephropathy, 39 T2DM patients without nephropathy, and 37 healthy subjects. Biochemical analysis was carried out on all participants and PCR method was utilized for genotyping the adiponectin polymorphism (rs1501229). Results: In the DN group, the genotype models frequencies were 22.2% for genotype (GG), 33.3% for heterozygous genotype (GT), and 44.4% for homozygous (TT), while the DM group had frequencies of 29.7% for GG, 51.3% for GT, and 23% for TT. When comparing the polymorphism between the control group and the DN group, T allele carriers had a high significant risk of DN under the codominant TT model (P = 0.01), the dominant GT + TT model (P = 0.04), and the recessive model (P = 0.01). In the T2DM group, the risk of DN was notably higher among T allele carriers under the recessive model (P = 0.04). Additionally, in the codominant model, the rs1501299 polymorphism genotypes were significantly associated with elevated levels of serum fasting blood sugar, HbA1c, urea, creatinine, and estimated glomerular filtration rate in the study participants. Conclusion: Our findings demonstrate a substantial association between the polymorphism (rs1501299) and an increased susceptibility to DN among individuals with T2DM in the Iraqi patient populatio

Abstract: Background: Growing evidence suggests the involvement of angiotensin-converting enzyme 2 (ACE2) in lipid metabolism and cardiovascular homeostasis. Genetic variations in ACE2 have been linked to metabolic disorders, including dyslipidemia, which is a hallmark of type 2 diabetes mellitus (T2DM). However, the association of ACE2 polymorphisms and dyslipidemia in T2DM patients, particularly in Iraqi populations, remains underexplored. Aim: This study aimed to investigate the association of ACE2 gene polymorphisms (rs2285666 and rs4646142) with dyslipidemia in Iraqi patients with T2DM, stratified by sex. Methods: A case-control study was conducted involving 463 T2DM patients (222 women and 241 men). Based on serum lipid profiles, participants were stratified into dyslipidemic (cases) and non-dyslipidemic (control) groups. Genotyping of ACE2 polymorphisms was performed using PCR-based methods, and serum ACE2 levels were quantified using ELISA. Results: The AA genotype of rs2285666 SNP was significantly associated with dyslipidemia in women (OR = 3.19, 95% CI = 1.31–7.78, p = 0.01), while the A allele was associated with dyslipidemia in men (OR = 2.36, 95% CI = 1.27–4.39, p = 0.006). High ACE2 levels, elevated atherogenic indices, and adverse lipid profiles were observed in carriers of the A allele. No significant association was found for rs4646142 SNP. Conclusion: The rs2285666 SNP was associated with dyslipidemia in Iraqi T2DM patients, with sex-specific differences in risk. The ACE2 variants may contribute to dyslipidemia pathogenesis in T2DM and highlight the potential for personalized risk stratification and therapeutic targets.

Abstract: Background: Growing evidence suggests the involvement of angiotensin-converting enzyme 2 (ACE2) in lipid metabolism and cardiovascular homeostasis. Genetic variations in ACE2 have been linked to metabolic disorders, including dyslipidemia, which is a hallmark of type 2 diabetes mellitus (T2DM). However, the association of ACE2 polymorphisms and dyslipidemia in T2DM patients, particularly in Iraqi populations, remains underexplored. Aim: This study aimed to investigate the association of ACE2 gene polymorphisms (rs2285666 and rs4646142) with dyslipidemia in Iraqi patients with T2DM, stratified by sex. Methods: A case-control study was conducted involving 463 T2DM patients (222 women and 241 men). Based on serum lipid profiles, participants were stratified into dyslipidemic (cases) and non-dyslipidemic (control) groups. Genotyping of ACE2 polymorphisms was performed using PCR-based methods, and serum ACE2 levels were quantified using ELISA. Results: The AA genotype of rs2285666 SNP was significantly associated with dyslipidemia in women (OR = 3.19, 95% CI = 1.31–7.78, p = 0.01), while the A allele was associated with dyslipidemia in men (OR = 2.36, 95% CI = 1.27–4.39, p = 0.006). High ACE2 levels, elevated atherogenic indices, and adverse lipid profiles were observed in carriers of the A allele. No significant association was found for rs4646142 SNP. Conclusion: The rs2285666 SNP was associated with dyslipidemia in Iraqi T2DM patients, with sex-specific differences in risk. The ACE2 variants may contribute to dyslipidemia pathogenesis in T2DM and highlight the potential for personalized risk stratification and therapeutic targets.