Pathophysiology of Obesity

Obesity is an exaggeration of normal adiposity and is a  central player in the pathophysiology of diabetes mellitus, insulin  resistance, dyslipidemia, hypertension, and atherosclerosis, largely  due to its secretion of excessive adipokines. Obesity is a major  contributor to the metabolic dysfunction involving lipid and glucose,  but on a broader scale, it influences organ dysfunction involving  cardiac, liver, intestinal, pulmonary, endocrine, and reproductive  functions. Inflammatory, insulin-resistant, hypertensive, and thrombotic-promoting adipokines, which are atherogenic, are counter- balanced by anti-inflammatory and anti-atherogenic adipocyte  hormones such as adiponectin, visfatin, and acylation-stimulating  protein, whereas certain actions of leptin and resistin are pro-atherogenic. Adiponectin is protective against liver fibrosis due to its anti-inflammatory effect, whereas inflammatory cytokines such as tumor  necrosis factor-α are detrimental for both fatty liver and pancreatic  insulin release. Obesity contributes to immune dysfunction from the  effects of its inflammatory adipokine secretion and is a major risk factor for many cancers, including hepatocellular, esophageal, and  colon. Because of the accelerating effects that obesity has on the  worsening of metabolic syndrome and cancer, it has the potential to  be profoundly detrimental to our species if major methods of prevention and/or effective treatment are not realized. It is essential then to institute major educational efforts aimed at promoting better eating habits and physical exercise