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. 2014 Mar 12;3(4):408–418. doi: 10.1016/j.molmet.2014.02.001

Figure 2.

Figure 2

Impaired mitochondrial function induces insulin resistance in 3T3L1 adipocytes. (A) Basal respiration; (B) Mitochondrial function; (C) Extracellular acidification rate (ECAR); (D) ATP concentration; (E) Basal and insulin-stimulated (10 nM) 2-deoxyglucose uptake; (F) Insulin action; (G) Insulin signalling; and (H) Basal and insulin-stimulated (10 nM) 2-deoxyglucose uptake in the presence or absence of MnTBAP in vehicle, 50 nM or 100 nM oligomycin treated (24 h) 3T3L1 adipocytes. (I) Basal respiration; (J) Mitochondrial function; (K) ECAR; (L) ATP concentration; (M) Basal and insulin-stimulated (10 nM) 2-deoxyglucose uptake; (N) Insulin action; and (G) Insulin signalling in vehicle, 1 nM or 5 nM rotenone treated (24 h) 3T3L1 adipocytes. Data presented as mean ± SEM, n = 3–6 biological replicates. Denotes significantly different from; † vehicle-treated cells, # vehicle/non-insulin-treated cells, * vehicle/insulin-treated cells (p < 0.05).