Figure 1.

Metabolic role for PLA2s. PLA2G1B is released by pancreatic acinar cells into the pancreatic juice following a meal and then secreted into the intestinal lumen, where it eventually becomes activated. Phospholipid digestion by PLA2G1B results in elevated lysophosphatidylcholine (LPC), lysophosphatidic acid (LPA), and free fatty acids absorption in the portal blood, plasma, and liver, and increases hepatic very-low density lipoprotein (VLDL) production. Elevated enzymatic activity in the intestinal lumen can progress obesity, reduce glucose tolerance, and exacerbate insulin resistance – most notably due to elevated release/absorption of LPC and overarching dyslipidemia. PLA2G2E and PLA2G5 are expressed in WAT. 2 studies have contradicting results in PLA2G2Es metabolic role – 1 study discovered PLA2G2E increases ERK1/2 signaling and HSL phosphorylation to increase lipolysis, whereas Study 2 found PLA2G2E may promote obesity through hepatic lipogenesis and VLDL production. PLA2G5 preferentially hydrolyzes PC-rich phospholipids and promotes M2 macrophage polarization, which appears to have a beneficial impact on LDL lipid normalization and whole-body insulin sensitivity.