Adipose Tissue (AT) is an endocrine organ with a key role in the regulation of the energy homeostasis. White AT accumulates energy in the form of triglycerides within lipid droplets and, therefore, is particularly abundant in obesity. In contrast, brown AT is specialized for energy expenditure playing a pivotal role on thermogenesis control and its mass decreases with obesity. AT secretes a large number of adipokines that regulate the central control of appetite and the metabolism of diverse peripheral tissues. This secretion and also the anatomical features of AT are closely related with the nutritional status and, naturally, strongly differ between normal weight and obese individuals. AT remodeling is indeed an ongoing process, that is pathologically exacerbated in the obese state. This review will discuss and present updated data describing the main changes in AT that correlate with an obese status. In obesity, AT changes in mass, capacity for energy storage, distribution through the organism, cellular composition, endocrine role and signaling. In summary, the chronic excess of nutrient supply leads to adipocyte hyperplasia and hypertrophy, hypoxia, mitochondrial dysfunction, proinflammatory signaling, adipokine secretion and, ultimately, to cell death. The extent of AT remodeling is closely associated with the pathophysiological consequences of obesity, including insulin resistance, cardiovascular disease, hypertension and hepatic steatosis.
Keywords: Adipocyte, Adipogenesis, Adipokines, Adipose tissue, Angiogenesis, Beige adipocyte, Brown adipose tissue, Crown-like structure, Fat, Fibrosis, Hyperplasia, Hypertrophy, Hypoxia, Inflammation, Insulin resistance, Lipid, Obesity, Oxidative stress, Subcutaneous adipose tissue, Visceral adipose tissue, White adipose tissue.