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. 2020 Aug 14;9:e52558. doi: 10.7554/eLife.52558

Figure 7. Conditional deletion of MPC1 in brown fat leads to compensatory increase in fatty acid oxidation.

(a) U-13C palmitate-tracing experiments in Mpc1F/F cells expressing CRE-ERT2. Cells were treated with ethanol or 4-hydroxy tamoxifen, with/without 100 nM CL-316,243 for 5 hours (N = 6). (b) Oxygen consumption rate in differentiated brown adipocytes treated with/without 100 nM CL-316,243 ± vehicle, 10 µM UK5099, 10 µM Etomoxir, or both (N = 10–12). (c) Oxygen consumption in mitochondria isolated from BAT of Mpc1F/F and Mpc1F/F::Ucp1Cre mice with 5 mM pyruvate and 0.5 mM malate or 5 mM L-Carnitine (N = 4). (d) Oxygen consumption in mitochondria isolated from BAT of Mpc1F/F and Mpc1F/F::Ucp1Cre mice with 1 mM ADP, 2 mM ascorbate and 0.5 mM TMPD (N = 4).

Figure 7.

Figure 7—figure supplement 1. Proton leak in response to UK5099, etomoxir, or both.

Figure 7—figure supplement 1.

(a) Seahorse analysis of proton leak in differentiated brown adipocytes treated with/without 100 nM CL-316,243 ± vehicle, 10 µM UK5099, 10 µM Etomoxir, or both (N = 10–12).