Abstract
Adipocytes not only function as energy depots but also secrete numerous adipokines that regulate multiple metabolic processes, including lipid homeostasis. Dysregulation of lipid homeostasis, which often leads to adipocyte hypertrophy and/or ectopic lipid deposition in non-adipocyte cells such as muscle and liver, is linked to the development of insulin resistance. Similarly, an altered secretion profile of adipokines or imbalance between calorie intake and energy expenditure is associated with obesity, among other related metabolic disorders. In lungs, lipid-laden adipocyte-like cells known as lipofibroblasts share numerous developmental and functional similarities with adipocytes, and similarly influence alveolar lipid homeostasis by facilitating pulmonary surfactant production. Unsurprisingly, disruption in alveolar lipid homeostasis may propagate several chronic inflammatory disorders of the lung. Given the numerous similarities between the two cell types, dissecting the molecular mechanisms underlying adipocyte development and function will offer valuable insights that may be applied to, at least, some aspects of lipofibroblast biology in normal and diseased lungs. FGF10, a major ligand for FGFR2b, is a multifunctional growth factor that is indispensable for several biological processes, including development of various organs and tissues such as the lung and WAT. Moreover, accumulating evidence strongly implicates FGF10 in several key aspects of adipogenesis as well as lipofibroblast formation and maintenance, and as a potential player in adipocyte metabolism. This review summarizes our current understanding of the role of FGF10 in adipocytes, while attempting to derive insights on the existing literature and extrapolate the knowledge to pulmonary lipofibroblasts.
Highlights
FGF10, a member of the FGF family, is a potent mitogen that is indispensable for proper development, regeneration, and health
Fischer et al (2017) reported the existence of a miRNA327-FGF10-FGFR2 autocrine regulatory loop in platelet-derived growth factor receptor α (PDGFRα)+ cells, which is critical for white adipose tissue (WAT) browning
Fgf10 overexpression in intramuscular adipocytes enhanced the expression of lipoprotein lipase (LPL) among other transcription factors, while Fgf10 knockdown using RNA interference suppressed the expression of LPL and LPL-induced lipid accumulation (Xu et al, 2018). These findings suggest a possible role for FGF10 in regulating adipocyte metabolism while raising the question of whether FGF10 would target LPL directly or via PPAR-γ to exert its effects in adipocyte metabolism
Summary
FGF10, a member of the FGF family, is a potent mitogen that is indispensable for proper development, regeneration, and health. Among the FGFs, Fgf is well-characterized for its roles in development of various organs and tissues, including the lung and white adipose tissue (WAT) (Gartside et al, 2009; Ohta and Itoh, 2014; Ornitz and Itoh, 2015). Mice lacking Fgf or its primary receptor Fgfr2b display multiple organ defects, including complete lung agenesis (Min et al, 1998; De Moerlooze et al, 2000; Ohuchi et al, 2000). FGF10 expression was observed in adipose tissue and has been strongly implicated in adipogenesis (Sakaue et al, 2002; Patel et al, 2005; Ohta and Itoh, 2014). We summarize the current knowledge and gaps in our understanding of the role of FGF10 in adipocytes and adipocytelike cells
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