PPARGC1A and Hyperglycemia: Our work in rodent models of type 1 and 2 diabetes has demonstrated that hyperglycemia triggers nutrient excess in neurons that, in turn, mediates a phenotypic change in mitochondria through alteration of the AMP-activated protein kinase (AMPK)/peroxisome proliferator–activated receptor γ coactivator-1α (PGC-1α) signaling axis [21].