LPL and endothelial dysfunction: Furthermore, in conditions of IR, reduced lipoprotein lipase activity and elevated hepatic TG lipase expression can lead to increased circulating TGs and reduced HDL-C, contributing to the atherogenic lipid profile commonly observed in HDP.[34–36] This constellation of lipid and protein imbalances provides a mechanistic explanation for the U-shaped relationship identified in our analysis: both inadequate protein synthesis and excessive lipid accumulation disrupt maternal vascular homeostasis, increase oxidative stress, and promote endothelial dysfunction.