Insulin resistance is a key factor in the development of cardiovascular disease (CVD). It is characterized by impaired insulin signaling, leading to defects in glucose uptake, glycogen synthesis, and lipid metabolism. Insulin resistance is associated with obesity, abnormal lipid profiles, and chronic hyperglycemia, which contribute to oxidative stress, inflammation, and endothelial dysfunction. These factors promote atherosclerosis, dyslipidemia, and the formation of atherosclerotic plaques. Insulin resistance also affects cardiac metabolism, leading to impaired glucose utilization, increased fatty acid oxidation, and lipid accumulation in the heart, which can result in cardiomyopathy and heart failure. The mechanisms linking insulin resistance to CVD include altered insulin signaling, impaired substrate metabolism, and reduced substrate delivery to the myocardium. Insulin resistance is associated with the lipid triad: high plasma triglycerides, low high-density lipoprotein (HDL), and the presence of small dense low-density lipoproteins (sdLDL). These factors, along with endothelial dysfunction, contribute to atherosclerosis. Insulin resistance also increases the risk of hypertension, which is linked to the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system overactivity. Insulin resistance is a major contributor to metabolic disorders such as type 2 diabetes, and it is associated with various clinical conditions, including breast cancer, rheumatoid arthritis, and non-alcoholic fatty liver disease. The development of insulin resistance is influenced by genetic factors, fat-derived signals, physical inactivity, obesity, and inflammation. Obesity, particularly visceral adiposity, is closely linked to insulin resistance and increased cardiovascular risk. Insulin resistance also leads to increased production of pro-inflammatory adipocytokines, which contribute to lipolysis, hepatic triglyceride synthesis, and hyperlipidemia. Insulin resistance affects the heart's ability to utilize glucose and fatty acids, leading to metabolic inflexibility and lipid accumulation. This can result in cardiomyopathy, impaired cardiac function, and reduced diastolic function. Insulin resistance also contributes to chronic hyperglycemia, which can lead to oxidative stress, endothelial dysfunction, and the development of diabetic complications such as retinopathy and nephropathy. The interplay between insulin resistance, dyslipidemia, and endothelial dysfunction further exacerbates the risk of CVD. In conclusion, insulin resistance plays a central role in the development of CVD through multiple mechanisms, including atheroma plaque formation, ventricular hypertrophy, and diastolic dysfunction. Understanding the molecular and cellular mechanisms of insulin resistance is crucial for developing new therapies to prevent and treat CVD.Insulin resistance is a key factor in the development of cardiovascular disease (CVD). It is characterized by impaired insulin signaling, leading to defects in glucose uptake, glycogen synthesis, and lipid metabolism. Insulin resistance is associated with obesity, abnormal lipid profiles, and chronic hyperglycemia, which contribute to oxidative stress, inflammation, and endothelial dysfunction. These factors promote atherosclerosis, dyslipidemia, and the formation of atherosclerotic plaques. Insulin resistance also affects cardiac metabolism, leading to impaired glucose utilization, increased fatty acid oxidation, and lipid accumulation in the heart, which can result in cardiomyopathy and heart failure. The mechanisms linking insulin resistance to CVD include altered insulin signaling, impaired substrate metabolism, and reduced substrate delivery to the myocardium. Insulin resistance is associated with the lipid triad: high plasma triglycerides, low high-density lipoprotein (HDL), and the presence of small dense low-density lipoproteins (sdLDL). These factors, along with endothelial dysfunction, contribute to atherosclerosis. Insulin resistance also increases the risk of hypertension, which is linked to the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system overactivity. Insulin resistance is a major contributor to metabolic disorders such as type 2 diabetes, and it is associated with various clinical conditions, including breast cancer, rheumatoid arthritis, and non-alcoholic fatty liver disease. The development of insulin resistance is influenced by genetic factors, fat-derived signals, physical inactivity, obesity, and inflammation. Obesity, particularly visceral adiposity, is closely linked to insulin resistance and increased cardiovascular risk. Insulin resistance also leads to increased production of pro-inflammatory adipocytokines, which contribute to lipolysis, hepatic triglyceride synthesis, and hyperlipidemia. Insulin resistance affects the heart's ability to utilize glucose and fatty acids, leading to metabolic inflexibility and lipid accumulation. This can result in cardiomyopathy, impaired cardiac function, and reduced diastolic function. Insulin resistance also contributes to chronic hyperglycemia, which can lead to oxidative stress, endothelial dysfunction, and the development of diabetic complications such as retinopathy and nephropathy. The interplay between insulin resistance, dyslipidemia, and endothelial dysfunction further exacerbates the risk of CVD. In conclusion, insulin resistance plays a central role in the development of CVD through multiple mechanisms, including atheroma plaque formation, ventricular hypertrophy, and diastolic dysfunction. Understanding the molecular and cellular mechanisms of insulin resistance is crucial for developing new therapies to prevent and treat CVD.