Obesity, metabolic dysfunction, and inflammation in polycystic ovary syndrome

Abstract

Obesity has grown in pandemic proportions with modern dietary habits and sedentary lifestyle as likely contributors. More recently, epigenetic phenomena have been implicated in the development of obesity. Beyond its energy-storing capacity, the adipose tissue acts as an endocrine and immunological organ. Accumulation of excess adiposity causes dysfunction of the adipose tissue compartment. This dysfunction ultimately leads to immune alterations characterized by inflammation, which then cause metabolic derangement and endocrine imbalance. Obesity increases the risk of developing type 2 diabetes mellitus (DM), dyslipidemia, and hypertension. In polycystic ovary syndrome (PCOS), the presence of obesity exacerbates the signs and symptoms of the disorder by worsening preexisting chronic low-grade inflammation and insulin resistance. In many ways, the metabolic pathophysiology of obesity and PCOS runs in parallel, except that the proinflammatory effects that promote metabolic dysfunction are more pronounced in obesity compared with what is observed in PCOS alone. Nevertheless, diet-induced oxidative stress and inflammation in PCOS that are independent of excess adiposity induce molecular alterations that may be the underpinning of insulin resistance, atherogenesis, and ovarian dysfunction in this disorder.