Four weeks of pioglitazone treatment attenuated HFD-induced glucose metabolic dysfunction, upregulated ventral hippocampal GFAP (glial fibrillary acidic protein), reduced the total process length and number of branching sites of hippocampus CA1 GFAP-immunoreactive astrocytes in the ventral hippocampus, and attenuated the depressive phenotype, suggesting that pioglitazone may be a promising therapeutic agent for metabolic disorders and related depression [68]. The gene discussed is GFAP; the disease is metabolic disease.