Pathophysiology of obesity

Pathophysiology of obesity Photo Obesity is an exaggeration of normal adiposity and is a central player in the pathophysiology of diabetes mellitus, insulin resistance, dyslipidaemia, 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 counterbalanced 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 tumour necrosis factor-? 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, oesophageal, and colon. 
  • Dysregulation of Lipid
  • Dysregulation Glucose Metabolism
  • Lipotoxicity

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