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. 2020 May 21;245(14):1268–1279. doi: 10.1177/1535370220928276

Figure 2.

Figure 2.

Intracellular metabolism of palmitate is required for mTORC1 activation and lipotoxic effects. (a) AML12 cells were pretreated either long-chain fatty acyl-CoA synthetase inhibitor (Triacsin C at 10 µM) for 2 h prior to palmitate exposure (0.4 mM). mTORC1 activation status was determined by Western blot detection of S6K1 and S6 protein phosphorylation after 16-h palmitate exposure; (b) Quantitative analysis of the ratios of p-S6K1 to S6K1 and p-S6 to S6 for the indicated treatments. All values are denoted as means ± SD from three or more independent experiments. Bars with different characters differ significantly (P < . 05); (c) AML12 cells were pretreated SCD-1 inhibitor GSK1940029 (20 µM) for 2 h before palmitate addition (0.4 mM). mTORC1 activation status was determined by Western blot detection of S6K1 and S6 protein phosphorylation after 16-h palmitate exposure; (d) Quantitative analysis of the ratios of p-S6K1 to S6K1 and p-S6 to S6 for the indicated treatments. All values are denoted as means ± SD from three or more independent experiments. Bars with different characters differ significantly (P < . 05).