Fig. 7: Schematic diagram illustrating the consequences of WAT browning and its associated lipotoxicity for the liver after a burn injury. | Cell Death & Disease

Fig. 7: Schematic diagram illustrating the consequences of WAT browning and its associated lipotoxicity for the liver after a burn injury.

From: Browning of white adipose tissue after a burn injury promotes hepatic steatosis and dysfunction

Fig. 7

Following a burn injury you have the activation of the browning process whereby the white adipose tissue converts to beige fat. Pro-inflammatory FFAs released from beige fat than travel to the liver causing hepatic steatosis and hepatic dysfunction by activating the ER stress response in hepatocytes. Hepatic ER stress then leads to increased expression of the MAM enriched protein IP3R1, which leads to a greater ER-Mitochondria interaction and facilitates Ca2+ transfer from ER (via IP3R1) to the mitochondria. This, in turn, can lead to reductions in mitochondrial fat oxidation. If this chronic ER stress mediated by lipid infiltration is not mitigated it can ultimately result in cellular apoptosis.

Back to article page