Abstract
Obesity is a growing health concern worldwide because of its contribution to metabolic syndrome, type II diabetes, insulin resistance (IR), and numerous cancers. In obesity, white adipose tissue (WAT) expands through two mechanisms: increase in adipocyte cell number by precursor cell differentiation through the process of adipogenesis (hyperplasia) and increase in existing mature adipocyte cell size (hypertrophy). While hypertrophy is associated with the negative effects of obesity on metabolic health, such as inflammation and lipotoxicity, adipogenesis prevents obesity-mediated metabolic decline. Moreover, in metabolically healthy obesity adipogenesis is increased. Thus, it is vital to understand the mechanistic basis for adipose expansion to inform novel therapeutic approaches to mitigate the dysfunction of this tissue and associated diseases. In this mini-review, we summarize recent studies on the regulation of adipogenesis and provide a perspective on targeting adipogenesis as a potential therapeutic avenue for metabolic disorders.
Highlights
Adiposity is linked to numerous diseases, adipocytes are critical for maintaining healthy systemic metabolism
Insulin engages the insulin receptor, activating the signaling cascade consisting of insulin receptor substrate (IRS), phosphoinositide 3-kinase (PI3K), AKT, and the mechanistic target of rapamycin complex 1 to promote glucose uptake into differentiating preadipocytes
Early mechanistic studies investigating the function of peroxisome proliferator-activated receptor γ (PPARγ) in adipogenesis were performed using in vitro model systems (Tontonoz et al, 1994; Rosen et al, 1999), the loss of white adipose tissue (WAT) in PPARγ-deficient mouse models such as chimeric PPARγ-null (Rosen et al, 1999), tetraploid rescued (Barak et al, 1999), and adipocyte-specific PPARγ knockouts (KOs) (Wang et al, 2013a) provide evidence for its role in adipogenesis in vivo
Summary
White adipose tissue (WAT) expands through two mechanisms: increase in adipocyte cell number by precursor cell differentiation through the process of adipogenesis (hyperplasia) and increase in existing mature adipocyte cell size (hypertrophy). While hypertrophy is associated with the negative effects of obesity on metabolic health, such as inflammation and lipotoxicity, adipogenesis prevents obesity-mediated metabolic decline. It is vital to understand the mechanistic basis for adipose expansion to inform novel therapeutic approaches to mitigate the dysfunction of this tissue and associated diseases. In this mini-review, we summarize recent studies on the regulation of adipogenesis and provide a perspective on targeting adipogenesis as a potential therapeutic avenue for metabolic disorders
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