Furthermore, both SR-A and LOX-1 mRNA and protein are increased in macrophages from mice with diabetes, again via mechanisms that point toward glucose being the culprit (30, 31), thus suggesting that the increase in lipid loading observed in diabetes may be in part due to intrinsic effects on uptake pathways which may be driven by hyperglycemia and or defective insulin signaling. This evidence concerns the gene OLR1 and diabetes mellitus.