For example, lipid-free apoA-I treatment increases glucose-stimulated insulin secretion (GSIS) in C57BL6 mice with diet-induced obesity, and in isolated islets from mice with elevated islet cholesterol levels and impaired insulin secretion due to the conditional deletion of the ATP binding cassette transporters, ABCA1 and ABCG1, which export cholesterol from β-cells to lipid-free/lipid-poor apoA-I and HDLs, respectively [24,26,27,79]. Here, APOA1 is linked to obesity due to melanocortin 4 receptor deficiency.