Abstract
The number of brown adipocytes residing within murine white fat depots (brite adipocytes) varies a lot by depot, strain and physiological condition. Several endocrine fibroblast growth factors are implicated in the regulation of brite adipocyte abundance. The family of fibroblast growth factors can be categorized by their site of action into endocrine, paracrine and intracellular peptides. We here screened paracrine fibroblast growth factors for their potential to drive brite adipogenesis in differentiating epididymal white adipocytes and identified fibroblast growth factor 8b to induce uncoupling protein 1 expression, but at the same time to interfere in adipogenesis. In an in vivo trial, fibroblast growth factor 8b released into the epididymal fat depot failed to robustly increase the number of brite adipocytes. The specific action of fibroblast growth factor 8b on the uncoupling protein 1 promoter in cultured epididymal adipocytes provides a model system to dissect specific gene regulatory networks.
Highlights
Brown adipose tissue (BAT) is an organ equipping mammals with a means of non-shivering thermogenesis
We obtained the respective peptides of recombinant murine or human origin to screen their potential to induce the expression of the brown adipocyte specific gene uncoupling protein 1 (Ucp1) in white adipocytes
Endocrine fibroblast growth factor 21 (FGF21) is a key regulator of substrate utilization and is able to recruit brite adipocytes in white adipose tissue[10,11]
Summary
Brown adipose tissue (BAT) is an organ equipping mammals with a means of non-shivering thermogenesis. To convert WAT into BAT by means of recruiting brite cells offers a possibility to massively increase the BAT amount accessible to therapeutic activation and at the same time would decrease the amount of WAT, thereby replacing an energy-storing organ with an energy-dissipating one This browning of white fat has been subject of intense research and several systemic interventions are known to increase at least to a certain degree the number of brite cells in mice, including cold exposure and treatment with beta-adrenergic agonists, cardiac natriuretic peptides or fibroblast growth factor 21 (FGF21)[7,8,9,10,11]. We investigated the potential of paracrine FGFs to re-route the differentiation of white preadipocytes towards brite mature adipocytes in the present study
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