The relationship between chronic changes in brain calcium homeostasis and metabolic dysfunctions such as hyperglycemia has been reported in obese mice; the signaling pathways dependent on the activation of Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII), which was induced by mitochondrial reactive oxygen species, and Ca2+ release from ER [43,44,45]. Here, CALM2 is linked to Hyperglycemia.