RESUMO
BACKGROUND: Diabetes mellitus (DM) poses a significant health challenge worldwide. The impact of a sedentary lifestyle in predicting and managing complications of diabetes represents an urgent need for health strategies. The objective of this study was to evaluate the lipid profile among normoglycemic and prediabetic Saudi office workers. METHODS: The research was a case-control study carried out in Makkah al-Mukarramah (Kingdom of Saudi Arabia, KSA). Seventy-five office worker volunteers between the ages of 19 and 45 years were recruited for the study. The participants were divided into two groups: a control group of non-diabetic normal subjects (NGT) and prediabetic subjects with impaired fasting plasma glucose and/or impaired glucose tolerance (IGT), based on the American Diabetes Association recommendations. Measurements of glucose, hemoglobin A1C (HbA1C), total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), and low-density lipoprotein (LDL) were performed using standard procedures and commercial kits. Statistical analysis was performed to compare the lipid profile in the two groups, and a P-value of <0.05 was considered statistically significant. RESULTS: A proportion (58.7%) of the office workers are prediabetics; prediabetic office workers had higher total cholesterol compared to the control group (p < 0.05). Triglyceride levels were higher in office workers with prediabetes compared to the normoglycemic group (p < 0.05). LDL levels were elevated in the prediabetic office workers compared to the control group (p < 0.05). CONCLUSION: Office employees with prediabetes exhibit elevated levels of cholesterol, triglycerides, and LDL. The disturbance in lipid profile may be linked to impaired glucose tolerance in individuals with a sedentary lifestyle, such as office workers.
RESUMO
BACKGROUND: Cardiovascular diseases (CVD) are important causes of death worldwide. Atherosclerosis is a chronic inflammatory disorder. It is the major cause of CVD and is manifested by ischemic heart disease or coronary artery disease (CAD). TNF-α is a pro-inflammatory cytokine that regulates immune response and promotes the development of atherosclerosis. Cytochrome p450 1B1 (CYP1B1) is an enzyme involved in the metabolism of endogenous and exogenous substrates. OBJECTIVES: This study aimed at examining the association of TNF-α rs1800629 G>A and CYP1B1 rs1056827 G>T gene polymorphisms with CAD susceptibility in an Indian cohort. METHODS: AS-PCR and direct DNA sequencing were used to examine the association of TNF-α rs1800629 G >A and CYP1B1 rs1056827 G>T gene polymorphism with CAD in an Indian cohort. A total of 100 clinically confirmed cases of CAD and 110 matched apparently healthy controls were genotyped. RESULTS: Allelic and genotypic frequencies did not deviate from Hardy-Weinberg equilibrium in the controls (p>0.05) for TNF-α G-308A and CYP1B1 rs1056827G>A. There was no significant difference between the TNF-α rs1800629 A>G genotype distribution between cases and controls (P-value >0.05). A significant difference was observed between the CYP1B1 rs1056827 G>T genotype distribution between CAD cases and controls (p<0.0003). Our result indicated that in the codominant model, the GA genotype of the CYP1B1 rs1056827 G>T was associated with CAD with OR= 2.21(1.17 to 4.15), RR=1.38(1.07 to 1.78), and p<0.013. In the dominant model, the (GA+AA) genotype was associated with CAD with OR=2.79(1.54 to 5.05) and p<0.007. The CYP1B1 rs1056827 'A' allele was associated with CAD with OR = 2.30 (1.55 to 3.42) and p< 0.0001. Our results indicated that TNF-α 1800629 gene polymorphism was strongly associated with hypercholesteremia (p<0.0009), HDL (p<0.0001), TGL (p<0.039), hypertension (p<0.0001), and smoking (p<0.0001) in patients with Coronary Artery Disease. Similar correlations of CYP1B1 rs1056827 genotypes were reported with cholesterol (p<0.020), HDL (p<0.002), LDL (p<0.006), hypertension (p<0.03), and smoking (p<0.005). CONCLUSION: It was reported that the GA genotype of the CYP1B1 rs1056827 G>T was strongly associated with susceptibility to Coronary Artery Disease with OR= 2.21(1.17 to 4.15)) and p<0.013, and similarly, its A allele was associated with predisposition to CAD with OR = 2.30 (1.55 to 3.42) and p< 0.0001. Our results indicated that TNF-α 1800629 gene polymorphism is not associated with predisposition to Coronary Artery Disease. Nevertheless, these results should be taken with caution and further validated with larger-scale studies before being introduced in the clinical setting.
