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Published on: May 4, 2021
Characterization of the transcriptional and functional effects of fibroblast growth factor-1 on human preadipocyte
Felicity S Newell1, Hua Su, Hans Tornqvist
1Centre for Diabetes and Endocrine Research, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland, Australia.
Insights
Fibroblast growth factor-1 (FGF-1) enhances human adipogenesis, improving insulin response and adiponectin secretion in preadipocytes. FGF-1 also activates ERK1/2 signaling, crucial for this process.
Area of Science:
- Cell Biology
- Endocrinology
- Metabolic Research
Background:
- Fibroblast growth factor-1 (FGF-1) was previously shown to promote adipogenesis.
- Human preadipocytes (phPA) and Simpson-Golabi-Behmel syndrome (SGBS PA) models were used to study adipogenesis.
- Murine 3T3-L1 preadipocyte cell line (3T3-L1 PA) served as a comparison model.
Purpose of the Study:
- To characterize the adipogenic effects of FGF-1 in primary human preadipocytes (phPA) and SGBS PA.
- To compare FGF-1's effects in human models versus murine 3T3-L1 PA.
- To investigate the role of extracellular regulated kinase 1/2 (ERK1/2) in FGF-1-induced adipogenesis.
Main Methods:
- Treatment of phPA, SGBS PA, and 3T3-L1 PA with FGF-1.
- Analysis of adipogenic marker gene expression (e.g., peroxisome proliferator-activated receptor-gamma).
- Assessment of insulin responsiveness and adiponectin secretion.
- Investigation of ERK1/2 phosphorylation and activity using inhibitors.
Main Results:
- FGF-1 upregulated the adipogenic program in phPA, increasing adipocyte markers and insulin responsiveness.
- phPA differentiated with FGF-1 showed increased adiponectin secretion.
- FGF-1 further enhanced differentiation in SGBS PA.
- Human phPA models did not exhibit mitotic clonal expansion, unlike 3T3-L1 PA.
- FGF-1 induced ERK1/2 phosphorylation, and ERK1/2 inhibition reduced phPA differentiation.
Conclusions:
- FGF-1 treated phPA represent a valuable in vitro model for studying human adipogenesis and insulin action.
- ERK1/2 activation is essential for human adipogenesis, independent of mitotic clonal expansion.
- FGF-1 promotes key aspects of adipogenesis and metabolic function in human preadipocytes.
Abstract:
We recently established that fibroblast growth factor (FGF)-1 promotes adipogenesis of primary human preadipocytes (phPA). In the current report, we have characterized the adipogenic effects of FGF-1 in phPA and also in a human PA strain derived from an individual with Simpson-Golabi-Behmel syndrome (SGBS PA), which exhibit an intrinsic capacity to differentiate with high efficiency. In further studies, we compared these models with the well-characterized murine 3T3-L1 preadipocyte cell line (3T3-L1 PA). FGF-1 up-regulated the adipogenic program in phPA, with increased expression of peroxisome proliferator-activated receptor-gamma in confluent PA prior to induction of differentiation and increased expression of adipocyte markers during differentiation. Moreover, phPA differentiated in the presence of FGF-1 were more insulin responsive and secreted increased levels of adiponectin. FGF-1 treatment of SGBS PA further enhanced differentiation. For the most part, the adipogenic program in phPA paralleled that observed in 3T3-L1 PA; however, we found no evidence of mitotic clonal expansion in the phPA. Finally, we investigated a role for extracellular regulated kinase 1/2 (ERK1/2) in adipogenesis of phPA. FGF-1 induced robust phosphorylation of ERK1/2 in early differentiation and inhibition of ERK1/2 activity significantly reduced phPA differentiation. These data suggest that FGF-1 treated phPA represent a valuable in vitro model for the study of adipogenesis and insulin action and indicate that ERK1/2 activation is necessary for human adipogenesis in the absence of mitotic clonal expansion.
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