Abstract
White adipose tissue (WAT) has key metabolic and endocrine functions and plays a role in regulating energy homeostasis and insulin sensitivity. WAT is characterised by its capacity to adapt and expand in response to surplus energy through processes of adipocyte hypertrophy and/or recruitment and proliferation of precursor cells in combination with vascular and extracellular matrix remodelling. However, in the context of sustained obesity, WAT undergoes fibro-inflammation, which compromises its functionality, contributing to increased risk of type 2 diabetes and cardiovascular diseases. Conversely, brown adipose tissue (BAT) and browning of WAT represent potential therapeutic approaches, since dysfunctional white adipocyte-induced lipid overspill can be halted by BAT/browning-mediated oxidative anti-lipotoxic effects. Better understanding of the cellular and molecular pathophysiological mechanisms regulating adipocyte size, number and depot-dependent expansion has become a focus of interest over recent decades. Here, we summarise the mechanisms contributing to adipose tissue (AT) plasticity and function including characteristics and cellular complexity of the various adipose depots and we discuss recent insights into AT origins, identification of adipose precursors, pathophysiological regulation of adipogenesis and its relation to WAT/BAT expandability in obesity and its associated comorbidities.
Highlights
Obesity and its metabolic complications (e.g. type 2 diabetes, cardiometabolic disorders) contributing to the metabolic syndrome represent one of the most important public health problems, with societal and economic implications urging for new therapeutic strategies and effective social policies
Obesity and its metabolic complications contributing to the metabolic syndrome represent one of the most important public health problems, with societal and economic implications urging for new therapeutic strategies and effective social policies
We discuss the current understanding of the origins of White adipose tissue (WAT), the identity of white/brown/brite adipocyte progenitors (APs) and how depot-specific vascularisation and fibro-inflammation interact with adipogenesis/cell hypertrophy, including the recent insights highlighted by lineagetracing studies in mice and genetic/genomics data obtained from humans
Summary
Obesity and its metabolic complications (e.g. type 2 diabetes, cardiometabolic disorders) contributing to the metabolic syndrome represent one of the most important public health problems, with societal and economic implications urging for new therapeutic strategies and effective social policies. We discuss the current understanding of the origins of WAT, the identity of white/brown/brite adipocyte progenitors (APs) and how depot-specific vascularisation and fibro-inflammation interact with adipogenesis/cell hypertrophy, including the recent insights highlighted by lineagetracing studies in mice and genetic/genomics data obtained from humans.
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