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. Author manuscript; available in PMC: 2020 Nov 1.
Published in final edited form as: Free Radic Biol Med. 2019 Jul 26;143:25–46. doi: 10.1016/j.freeradbiomed.2019.07.024

Figure 9. Lipolysis products decreased mitochondrial respiratory reserve capacity.

Figure 9.

HBMECs were injected port A-D with (1) lipolysis products for 30 min and followed by (2) 1 μM Oligomycin, (3) 1 μM FCCP, and (4) 0.5 μM rotenone combined with 0.5 μM antimycin A were added sequentially to measure cellular respiration parameters (basal respiration, maximal respiration, spare respiratory capacity and non-mitochondrial respiration). A mitochondrial respiration measurement of oxygen consumption rate (OCR) was performed during acute TGRL lipolysis products treatment using the XF Cell miniplate Seahorse system. A) Raw trace of OCR regulated by lipolysis products; B) reduced mitochondrial respiration or oxygen consumption; C) reduced ATP production; D) increased proton leak compared to media control treatment; E) Profile of Aglient Seahorse XF Mito stress test. N = 6 wells/treatment group and values are expressed as means ± SEM, *P≤0.05, compared to control group at the same time point.