In addition, a recent study demonstrated that macrophages from diabetic Ldlr−/− mice presented reduced GLUT1 expression and glycolysis compared with nondiabetic mice, suggesting that increased glucose uptake by tissue-resident macrophages is unlikely to contribute to plaque progression in diabetic atherosclerosis and that factors other than hyperglycemia, such as insulin, may contribute to macrophage metabolic alterations at the tissue level [54]. Here, SLC2A1 is linked to Hyperglycemia.