Obesity significantly increases the risk of developing type 2 diabetes, hypertension, coronary heart disease, stroke, fatty liver disease, dementia, obstructive sleep apnea and several types of cancer. Adipocyte and adipose tissue dysfunction represent primary defects in obesity and may link obesity to metabolic and cardiovascular diseases. Adipose tissue (AT) dysfunction manifests by a proinflammatory adipokine secretion pattern that mediate auto/paracrine and endocrine communication and by inflammatory cell infiltration, particularly in intra-abdominal fat. Impaired AT function is caused by the interaction of genetic, behavioral and environmental factors which lead to adipocyte hypertrophy, ectopic fat accumulation, hypoxia, AT stresses, impaired AT mitochondrial function and inflammatory processes within adipose tissue. Recently, increased autophagy has been linked to obesity and AT dysfunction and may represent a mechanism to compensate for AT stresses. A better understanding of mechanisms causing or maintaining AT dysfunction may provide new therapeutic strategies in the treatment of obesity-induced metabolic diseases.
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