However, in an experimental model in vivo, the increased glucose uptake did not stimulate inflammatory activation of peritoneal cells upon ex vivo stimulation with LPS, neither did it affect the development of atherosclerosis in Ldlr−/− mice in vivo [71], suggesting that increased glucose supply alone is not sufficient to drive inflammatory activation and atherosclerosis in non-activated myeloid cells [72]. Here, LDLR is linked to atherosclerosis.