| First Author | Fang D | Year | 2019 |
| Journal | Metabolism | Volume | 98 |
| Pages | 16-26 | PubMed ID | 31132382 |
| Mgi Jnum | J:289429 | Mgi Id | MGI:6435051 |
| Doi | 10.1016/j.metabol.2019.05.008 | Citation | Fang D, et al. (2019) The glycoprotein follistatin-like 1 promotes brown adipose thermogenesis. Metabolism 98:16-26 |
| abstractText | OBJECTIVES: The thermogenic brown adipose tissue (BAT) has been proposed as a potential target to prevent or treat obesity and related metabolic diseases. BAT secretes adipokines to regulate the thermogenic program in an autocrine or paracrine manner. Follistatin-like 1 (FSTL1), a glycoprotein involved in adipogenesis and obesity, however, the function of FSTL1 in BAT thermogenesis and in the regulation of systemic energy homeostasis are not fully understood. METHODS: Whole-body ablation Fstl1 heterozygous mice (Fstl1(+/-)) and its littermates control were injected with CL316,243 to assess energy balance. A series of FSTL1 overexpression and knockdown experiments were carried out to evaluate its function in regulating thermogenic gene expression in brown adipocytes. RESULTS: FSTL1 expression was induced upon BAT activation during cold challenge or beta3-adrenergic activation. FSTL1 haploinsufficiency in mice led to reduced thermogenic gene expression, impaired BAT recruitment, and decreased heat production. FSTL1 cell-autonomously promoted the beta3-adrenergic signaling, which was required to upregulate PPARgamma and UCP1 in brown adipocytes. Furthermore, only glycosylated FSTL1 could be secreted from brown adipocytes to induce the beta3-adrenergic activation. CONCLUSIONS: Our results suggest FSTL1 as a novel stimulator of the beta-adrenergic signaling and BAT thermogenesis. |
