LCAT and Insulin resistance: Indeed, both hyperglycemia and insulin resistance have been shown to impact HDL particles in different ways: by altering the HDL subspecies proportion in favor of the small-dense HDL3 with respect to the large HDL2; by altering the HDL proteome; by modifying the enzymatic activity of HDL-associated proteins, such as ﻿lecithin-cholesterol acyltransferase (LCAT) and paraoxonase-1 (PON-1); by increasing HDL hepatic catabolism through an enhanced activity of hepatic lipase; and by reducing their anti-inflammatory activity mediated by apolipoprotein A1 (ApoA-I) [13–17].