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. 2021 Nov 2;22(21):11881. doi: 10.3390/ijms222111881

Figure 4.

Figure 4

(A) Mitochondrial function as judged by changes in non-mitochondrial respiration, basal respiration, maximal respiration, proton leak-related respiration, ATP production-linked respiration, spare respiratory capacity and coupling efficiency (CE) determined from the oxygen consumption rate (OCR) in response to subsequent addition of oligomycin (O), FCCP and rotenone (R)/antimycin A (A) as indicated in the left panel of control and 24 h mammary adipose tissue co-cultured E0771 cells. Data are presented as OCR normalized to total protein levels (N = 30/group). (B) Glycolytic function, as determined by basal glycolysis rate, glycolytic capacity and glycolytic reserve, was estimated from the extracellular acidification rate (ECAR) of control and 24 h mammary adipose tissue co-cultured E0771 cells in response to subsequent addition of glucose (G), oligomycin (O) and 2-Deoxy-D-glucose (2-DG) as indicated in the left panel. Data are presented as ECAR normalized to total protein levels (N = 30/group). (C) Endogenous and (D) exogenous fatty acid oxidation estimated from the OCR of control and 24 h mammary adipose tissue co-cultured E0771 cells under low-glucose conditions (1.5 mM glucose, with or without the carnitine palmitoyltransferase-1 (CPT-1) inhibitor Etomoxir (eto), with or without BSA-conjugated palmitate (PA:BSA) in response to subsequent addition of oligomycin (O), FCCP and rotenone (R)/antimycin A (A) as indicated in the left panel A (N = 12/group). Data are presented as mean ± SEM; * p < 0.05, ** p < 0.01 and ***p < 0.001.