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. Author manuscript; available in PMC: 2017 Aug 9.
Published in final edited form as: Cell Metab. 2016 Aug 9;24(2):246–255. doi: 10.1016/j.cmet.2016.07.004

Figure 1.

Figure 1

Mitochondrial respirometry in human and rodent white and brown adipose tissue. (a) Representative respiration experiments performed on permeabilized sWAT and sBAT from humans following the sequential titration of substrates (1.5 mM octanoyl-l-carnitine, 5 mM pyruvate, 2 mM malate, 10 mM glutamate), 20 mM of the UCP1 inhibitor GDP and 5 μM of the protonophore CCCP (values are group means). (b) Comparison of respiratory states (state 2, State 2GDP, and State 2U) for human sWAT and sBAT shown in panel a. (c) UCP1-dependent respiration in human sWAT and sBAT calculated as the change in respiration following titration of the UCP1 inhibitor GDP. (d) Representative respiration experiments performed on permeabilized iWAT and iBAT from mice as described in panel a. (e) Comparison of respiratory states (state 2, State 2GDP, and State 2U) for mouse iWAT and iBAT shown in panel d. (f) UCP1-dependent respiration in mouse iWAT and iBAT calculated as in c. Note that leak respiration prior to titration of substrates is supported by endogenous substrates, likely FFAs. Values are presented as group means ± SEM unless otherwise stated. *P<0.05, **P<0.01, and **P<0.001 vs. WAT.