Fig. 5
From: The role of HIF-1 in oncostatin M-dependent metabolic reprogramming of hepatic cells
Metabolic effects of PDK1 silencing on the OSM-induced metabolic phenotype in three PH5CH hepatocyte clones. a PDK1 mRNA expression in PH5CH8 cells. Fold changes were calculated relative to PDK1 expression in control samples under normoxia or hypoxia, respectively. b PDK1 protein expression in PH5CH8 cells. c PDH activity in PH5CH8 cells determined by the ratio of M2 isotopologues of citrate to M3 isotopologues of lactate, from [13C6]glucose. d Reductive glutamine contribution to citrate in PH5CH8 immortalized hepatocytes, determined by the ratio of M5 isotopologues of citrate to M5 isotopologues of glutamate, from [13C5]glutamine. e PDK1 mRNA and f protein levels in PH5CH1 and PH5CH7 cells under normoxia. g PDH activity under normoxia in PH5CH1 and PH5CH7 cells determined by the ratio of M2 isotopologues of citrate to M3 isotopologues of lactate, from [13C6]glucose. h Reductive glutamine contribution to citrate under normoxia in PH5CH1 and PH5CH7 immortalized hepatocytes, determined by the ratio of M5 isotopologues of citrate to M5 isotopologues of glutamate, from [13C5]glutamine. Metabolites were extracted after 36 h of indicated treatment. All error bars indicate the standard deviation. All p values and error bars are calculated from at least three independent replicates (n>=3). Statistical significance was determined in comparison to the untreated control. * P<=0.05, ** P<=0.01, and *** P<=0.001