Abstract
Adipose tissue (AT) is comprised of a diverse number of cell types, including adipocytes, stromal cells, endothelial cells, and infiltrating leukocytes. Adipose stromal cells (ASCs) are a mixed population containing adipose progenitor cells (APCs) as well as fibro-inflammatory precursors and cells supporting the vasculature. There is growing evidence that the ability of ASCs to renew and undergo adipogenesis into new, healthy adipocytes is a hallmark of healthy fat, preventing disease-inducing adipocyte hypertrophy and the spillover of lipids into other organs, such as the liver and muscles. However, there is building evidence indicating that the ability for ASCs to self-renew is not infinite. With rates of ASC proliferation and adipogenesis tightly controlled by diet and the circadian clock, the capacity to maintain healthy AT via the generation of new, healthy adipocytes appears to be tightly regulated. Here, we review the contributions of ASCs to the maintenance of distinct adipocyte pools as well as pathogenic fibroblasts in cancer and fibrosis. We also discuss aging and diet-induced obesity as factors that might lead to ASC senescence, and the consequences for metabolic health.
Highlights
Adipose tissue (AT) is a highly dynamic organ that mediates glucose and lipid homeostasis.The expansion of white adipose tissue (WAT) is a hallmark of obesity, and visceral adipose tissue (VAT) dysfunction, in particular, is thought to help fuel metabolic syndromes, type-2 diabetes (T2D), cardiovascular disease, and cancer [1]
A number of studies have supported the idea that weight gain induces a new threshold of the adipocyte number that cannot be reversed even in the context of weight loss [29,62]. What regulates this observed hyperplasia under conditions of WAT expansion? To determine factors that contribute to hyperplasia in AT, a recent study identified TGFβ3, a protein that is released in the stromal vascular fraction of subcutaneous adipose tissue (SAT), as a factor which stimulates the proliferation of adipocyte precursors and regulates the number of fat cells in vivo [63]
The idea that the circadian clock might serve as a daily signal for preadipocyte proliferation is intriguing, though not one that has been directly addressed in mammalian models to date
Summary
Adipose tissue (AT) is a highly dynamic organ that mediates glucose and lipid homeostasis. Population ofnutrient cells: adipose progenitor cells/stromal cells (ASCs), endothelial cells (AECs), The turnover of adipocytes and pre-adipocytes in mice is higher than in humans [21,31]. It has and infiltrating hematopoietic cells [23]. Adipocyte hypertrophy leads to hypoxia and cell death, resulting in the recruitment of inflammatory leukocytes [34] When this chronic process becomes chronic in obesity or aging, it results in inflammation, fibrosis, and lipid spillover (Figure 1B). A better understanding of how APC capacity to generate new adipocytes is regulated is essential for the development of new approaches for the prevention of metabolic disease
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