Figure 3.

Effect of increased glucose on LDL-C metabolism and insulin secretion. In enterocytes, the increase in plasma glucose causes a decrease in cholesterol excretion consecutive to the reduction in the expression of ABCG5 and ABCG8. On the other hand, there is an increase in cholesterol absorption as a result of the high expression of NPC1L1. Both mechanisms contribute to raised plasma LDL-C levels. The increase in plasma glucose also reduces expression of LDLR in hepatocytes, another mechanistic pathway contributing to the increased plasma concentration of LDL-C. Such elevated plasma LDL-C levels together with the high expression of LDLR in pancreatic beta cells stimulate insulin secretion [2]. LDLR: LDL receptor, ABCG5/8: ATP Binding Cassette Subfamily G Member 5/ABCG8: ATP Binding Cassette Subfamily G Member 8, NPC1L1: Niemann–Pick C1-like 1 protein, LDL-C: LDL cholesterol.