These observations are supported by: 1) our recent publication indicating that treated type 2 diabetic mice with endoplasmic reticulum stress inhibitor reduced body weight and blood glucose and insulin levels [30], and 2) the occurrence of endoplasmic reticulum stress in endothelial cells in metabolic diseases [31–33], emphasizing that endoplasmic reticulum stress is a potential mechanism that contributes to the reduced nitric oxide release and bioavailability, which leads to vascular endothelial dysfunction. This evidence concerns the gene INS and Endoplasmic Reticulum Stress.