Adipose Structure (White, Brown, Beige)

Abstract

Our understanding of adipose tissue physiology and pathophysiology has substantially increased during the last decade. Notably, white adipose tissue (WAT) dysfunction has been proposed as a key determinant of obesity-associated metabolic complications. WAT is a complex metabolic organ composed of many cell types, including adipocytes as the main cell type involved in energy storage. Adipocytes also synthesize numerous molecules involved in the regulation of energy balance, vascular homeostasis, and insulin sensitivity. In obesity, WAT expansion is associated with intensified structural remodeling that compromises the tissue’s metabolic and secretory functions. Failure to efficiently store lipids in WAT results in a “spillover” of the excess of lipids into non-adipose tissues, which further disrupts metabolic homeostasis and contributes to the development of obesity-related pathologies, known collectively as metabolic syndrome. In contrast, brown adipose tissue (BAT) is an energy-dissipating thermogenic organ that produces heat by uncoupling mitochondrial fatty acid oxidation. Activation of BAT thermogenesis can ameliorate the effects of WAT dysfunction in metabolically compromised mouse models. The recent rediscovery of BAT in humans has raised the possibility that BAT could be a therapeutic target for metabolic syndrome. In this chapter, we will discuss important structural and cellular features of the WAT and BAT and how obesity alters WAT and BAT structure and function. , Abstract Our understanding of adipose tissue physiology and pathophysiology has substantially increased during the last decade. Notably, white adipose tissue (WAT) dysfunction has been proposed as a key determinant of obesity-associated metabolic complications. WAT is a complex metabolic organ composed of many cell types, including adipocytes as the main cell type involved in energy storage. Adipocytes also synthesize numerous molecules involved in the regulation of energy balance, vascular homeostasis, and insulin sensitivity. In obesity, WAT expansion is associated with intensified structural remodeling that compromises the tissue’s metabolic and secretory functions. Failure to efficiently store lipids in WAT results in a “spillover” of the excess of lipids into non-adipose tissues, which further disrupts metabolic homeostasis and contributes to the development of obesity-related pathologies, known collectively as metabolic syndrome. In contrast, brown adipose tissue (BAT) is an energy-dissipating thermogenic organ that produces heat by uncoupling mitochondrial fatty acid oxidation. Activation of BAT thermogenesis can ameliorate the effects of WAT dysfunction in metabolically compromised mouse models. The recent rediscovery of BAT in humans has raised the possibility that BAT could be a therapeutic target for metabolic syndrome. In this chapter, we will discuss important structural and cellular features of the WAT and BAT and how obesity alters WAT and BAT structure and function.