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

Figure 1.

Figure 1

Diverse models of cell-autonomous insulin resistance in 3T3L1 adipocytes is not associated with a common perturbation in mitochondrial function. (A) Basal and insulin-stimulated (10 nM) 2-deoxyglucose uptake; (B) Insulin signalling; (C) LDH release; (D) Oxygen consumption due to basal respiration, ATP turnover and H+ leak; (E) Mitochondrial membrane potential (MMP); and (F) Mitochondrial ROS production, in vehicle (Veh), glucose oxidase (G.O.; 25 mU/mL), TNFα (10 ng/mL) and chronic insulin (10 nM) treated (24 h) cells. Data presented as mean ± SEM, n = 3–6 biological replicates. Denotes significantly different from; # vehicle/non-insulin-treated cells, * vehicle/insulin-treated cells; and † vehicle-treated cells (p < 0.05).