EC Clinical and Medical Case Reports

Obesity, high blood pressure, inadequate glucose tolerance, and dyslipidemia are all components of the metabolic syndrome, which is a risk factor for cardiovascular disease (CVD) [1].

The malfunction of adipose tissue is associated with the prevalence of obesity accompanied by insulin resistance, hypertension, and cardiovascular disease because adipose tissue secretes a number of adipokines that regulate insulin sensitivity, energy metabolism, and vascular homeostasis [2]. Due to the enlargement of adipose tissue, obesity is believed to change the expression of adipokines, such as adiponectin, which has a strong anti-inflammatory and vascular protective effect [3]. Adiponectin is the most abundant adipose-specific adipokine. The heart, liver, pancreatic -cells, brain, bone, kidneys, blood vessels, immune cells, and many more tissues are all affected favorably by the adipokine [4]. Adiponectin provides protection the vasculature by acting pleiotropically on endothelial cells, endothelial progenitor cells, smooth muscle cells, and macrophages to increase insulin sensitivity and metabolic characteristics and inhibit the vascular dysfunction caused by obesity and diabetes [5,6]. Adhesion molecules in artery endothelial cells cause the buildup of monocytes/macrophages and T lymphocytes in atherosclerosis, an inflammatory disease [7]. Oxygen-derived free radicals (ROS) are one of the variables causing endothelial dysfunction, and adipocyte hypertrophy, one of the mechanisms underlying obesity, which is a low-grade inflammatory state, increases their levels [8]. Endoplasmic reticulum (ER) stress and mitochondrial malfunction are caused by this disorder [9].

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