Association between high-density lipoprotein subfractions and low-grade inflammation, insulin resistance, and metabolic syndrome components: The ELSA-Brasil study

In the metabolic syndrome setting, there is a lower apo A1 liberation from chylomicrons due to inhibition of lipoprotein lipase (1), reducing HDL formation. Also, CETP is activated (2) and leads to more significant enrichment of HDL with triglycerides, rendering this lipoprotein a better substrate for lipolysis by hepatic lipase (3 - thicker arrows), leading to the formation of smaller HDLs. Finally, there is less apoA1 production and HDL formation by hepatocytes (4). As a result, we observe less total HDL-C, HDL2-C, HDL3-C and lower values of HDL2-C/HDL3-C ratio