RESUMO
Type 2 diabetes mellitus (T2DM) and its complications are linked to environmental, clinical, and genetic factors. This review analyses the disorders of lipids and their genetics with respect to coronary artery disease (CAD) associated with T2DM. Cell organelles, hepatitis C-virus infection, reactive oxygen species produced in mitochondria, and defective insulin signaling due to the arrest of G1 phase to S phase transition of ß-cells have significant roles in the precipitation of the diseases. Adiponectin is anti-inflammatory and anti-atherosclerotic and improves insulin resistance. Low-density lipoprotein (LDL) is atherosclerotic, and LDL-cholesterol in T2DM is associated with high-cardiovascular risk. Further, LDL cholesterol reduction significantly reduces cardiovascular morbidity and mortality. High-density lipoprotein (HDL) is also anti-atherosclerotic due to HDL associated paraoxonase-1 serum enzyme, which prevents LDL oxidative modifications and the development of CAD. Moreover, elevated apolipoprotein B and apolipoprotein A-I (ApoB/ApoA-I) ratio in plasma is also a risk factor for CAD. LDL receptor, adiponectin, and endocannabinoid receptor-1 genes are independently associated with CAD and T2DM. Polymorphism of Apo E2 (epsilon2) is a positive factor to increase the T2DM risk and Apo E4 (epsilon4) is a negative factor to reduce the disease risk. Taq 1B polymorphism of cholesterol ester transfer protein (CETP) gene contributes to the development of atherosclerosis, whereas haplotypes of APOA5, APOC3, APOC4, and APOC5 genes are in the same cluster and are independently associated with high plasma triglyceride level, CAD and T2DM. In conclusion, because various genes, LDLR, CETP, APOA5, Apo E, Apo B, and Apo A-I, are associated with the precipitation of CAD associated with T2DM, a personalized diet-gene intervention therapy may be advocated to reduce the disease precipitation.
Assuntos
Doença da Artéria Coronariana/complicações , Diabetes Mellitus Tipo 2/complicações , Dislipidemias/complicações , Adiponectina/genética , Adiponectina/metabolismo , Apolipoproteína A-V , Apolipoproteína C-III/genética , Apolipoproteína E2/genética , Apolipoproteína E4/genética , Apolipoproteínas A/genética , Apolipoproteínas C/genética , Arildialquilfosfatase/metabolismo , Proteínas de Transferência de Ésteres de Colesterol/genética , HDL-Colesterol/metabolismo , LDL-Colesterol/metabolismo , Dislipidemias/genética , Dislipidemias/metabolismo , Pontos de Checagem da Fase G1 do Ciclo Celular , Hepatite C/metabolismo , Humanos , Mitocôndrias/metabolismo , Polimorfismo Genético , Espécies Reativas de Oxigênio/metabolismo , Receptor CB1 de Canabinoide/genética , Receptores de LDL/genética , Fatores de RiscoRESUMO
BACKGROUND: The metabolic syndrome (MS) (syndrome X, insulin resistance syndrome) is a constellation of metabolic abnormalities and a complex predisease state that predicts future development of type 2 diabetes mellitus and cardiovascular disease. Menopausal transition and postmenopausal state are considered as a vulnerable period for developing MS, and this increased risk has been attributed to decreasing estrogen levels with an increasing risk of insulin resistance following menopause. AIMS AND OBJECTIVES: This study aimed to determine the prevalence of MS and its components in pre- and post-menopausal women from North India. METHODOLOGY: This is a cross-sectional study of 350 women in the age group of 45-55 years attending gynecology clinic in a tertiary center of North India. Details of sociodemographic data, menopausal history, reproductive, and medical profile were obtained. Then, waist circumference, body mass index (BMI), and blood pressure were recorded. A venous blood sample was collected for fasting blood glucose, triglycerides, total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol. MS was defined according to the modified National Cholesterol Education Program Adult Treatment Panel III criteria. RESULTS: The mean age was 49.09 ± 2.2 years in premenopausal and 49.54 ± 2.8 years in postmenopausal women. The prevalence of MS in the study group was 62.6%. Occurrence of MS was higher in older and obese women. Abnormal waist circumference was the most prevalent component (87%) of MS and in terms of odd ratio, correlation was highest for BMI followed by total cholesterol and waist-hip ratio. CONCLUSION: We should target obesity and deranged lipid profile by bringing out changes in lifestyle and dietary habits to decrease the higher prevalence of MS and the risk of cardiovascular diseases.