Skip to main content
. 2015 Apr 29;156(7):2470–2481. doi: 10.1210/en.2014-2001

Figure 4.

Figure 4.

Central FGF21 is dependent on the SNS. The β-blocker propranolol counters the influence of FGF21 on IWAT and β-adrenoceptors are required for FGF21-mediated induction of BAT-specific markers, thermogenesis, and fatty acid oxidation in IWAT. IWAT of 5-day icv administration (0.4 μg/d) of FGF21 fails to induce gene expression of a panel of markers of browning in IWAT if the mice (n = 7 per group) are treated with the general β-blocker propranolol (A), but this is largely overcome if administered a large sc-FGF21 dose (24 μg/d) (vehicle, n = 6, FGF21 n = 8) plus propranolol (B). Mice lacking the β1, β2, and β3 adrenoceptors (β-less mice) fail to induce a browning profile in IWAT if given FGF21 (0.4 μg/d) icv (vehicle, n = 9, FGF21, n = 8) (C) or if administered a large sc-FGF21 dose (24 μg/d) to β-less mice (vehicle, n = 7, FGF21, n = 6) (D). Primary IWAT culture derived from β-less mice was unresponsive to vehicle or FGF21 treatment but did induce Ucp1 when treated with forskolin (E). Graphs are shown as mean ± SEM. *, P < .05; **, P < .01 by Student's t test.