As a result, HDL from APOA1-null (Apoa1−/−) mice contained primarily APOE, and HDL from LCAT-null (Lcat−/−) mice contained mainly APOA2; both strains had significantly reduced HDL-C levels, although only Apoa1−/− mice were presented with a T2DM phenotype because of the reduced ability of pancreatic β-islets to secrete insulin in response to glucose stimulation and the reduced skeletal muscle glucose uptake in response to insulin [25]. Here, LCAT is linked to type 2 diabetes mellitus.