In ob/ob and adipo-/- ob/ob mice, serum-free fatty acid and triglyceride levels, along with adipocyte sizes, remain stable after administering 10 mg/kg of Pioglitazone but significantly decrease following a 30 mg/kg dose. Similarly, levels of TNFα and resistin in the adipose tissues of these mice do not change with 10 mg/kg Pioglitazone but are reduced after 30 mg/kg. Consequently, Pioglitazone's mitigation of insulin resistance and diabetes appears to be adiponectin-dependent in the liver and independent in skeletal muscle^[3].

Pioglitazone (10 mg/kg per day) notably reduces body weight loss and cardiac hypertrophy, lowers elevated serum glucose levels, and improves dyslipidemia. It slightly increases serum creatinine levels in diabetic rats compared to normals, with marked renal dysfunction observed in the diabetic nephropathic group. Pioglitazone also reduces elevated serum levels of creatinine and creatine kinase-MB (CK-MB)^[4].

Pioglitazone completely eliminates beta cell necrosis induced by AGEs when added to the AGEs culture medium. Additionally, Pioglitazone fully inhibits any increase in caspase-3 activation caused by AGEs, thus returning caspase-3 activity to levels observed in control cells. As anticipated, AG effectively counteracts the viability impairment induced by AGEs^[2].