The mechanisms linking SD and abnormal glucose metabolism lie in several aspects: (1) the activation of the sympathetic nervous system can lower β-cells responses to glucose, thus resulting in reduced insulin sensitivity; (2) increasing free fatty acids brought by SD via promoting gluconeogenesis can lead to insulin resistance and hyperglycemia; and (3) the inflammation caused by SD, as mentioned above, can lead to insulin resistance, mainly via cytokines and corresponding signaling pathways (TNF-α & IKKβ/NF-κB pathway, IL-6 & JAK-STAT pathway) [107,108]. This evidence concerns the gene SOAT1 and Insulin resistance.