SLC31A1 and diabetes mellitus: Recent cell and mouse studies have demonstrated that excess advanced glycosylation end-products (AGEs) and copper in patients with diabetes cause the upregulation of ATF3/SPI1/SLC31A1 signaling, leading to downregulation of the mitochondrial respiratory chain complex, a reduction in ATP production, and inhibition of the activity of mitochondrial complexes I and III, resulting in cardiac cytotoxicity (12–14).