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. 2023 Feb 28;324(5):G341–G353. doi: 10.1152/ajpgi.00163.2022

Figure 7.

Figure 7.

The ATF4-CD36 pathway activation contributes to palmitate-induced lipotoxicity in hepatocytes. A and B: AML-12 cells were transfected with either scramble siRNA (si-Ctrl) or Atf4 siRNA (si-Atf4) for 24 h before palmitate exposure (0.4 mM) for 16 h. LDH release (A) and intracellular TAG contents (B) were measured. Student’s t test was used for statistical evaluation (**P < 0.01; ****P < 0.0001). C–F: AML-12 cells were transfected with either scramble siRNA (si-Ctrl) or Cd36 siRNA (si-Cd36) for 24 h before palmitate exposure (0.4 mM) for 16 h. Cd36 gene expression (C), LDH release (D), intracellular TAG contents (E), and de novo lipogenic genes (F) were measured. Student’s t test was used for statistical evaluation (**P < 0.01; ***P < 0.001; ****P < 0.0001). G: schematic illustration of the role of the ATF4-CD36 pathway activation in palmitate-induced hepatocyte lipotoxicity. ATF4, activating transcription factor 4; CD36, cluster of differentiation 36; TAG, triacylglycerol.