Diabetic KKAy mice exhibit increased hepatic PPARγ1 gene expression and develop hepatic steatosis upon chronic treatment with antidiabetic thiazolidinediones

摘要: Abstract Background/Aims : Peroxisome proliferator-activated receptor- γ , which is involved in the regulation of lipid homeostasis, upregulated liver obese and diabetic mice, but biological consequences this induction are largely unknown. This study was aimed at further characterizing upregulation exploring downstream effects specific activators on hepatic metabolism. Methods Hepatic expression peroxisome 1 2 mRNA protein analyzed by real-time polymerase chain reaction Western immunoblotting KKA y mice ob/ob mice. were treated with thiazolidinediones, triglyceride content distribution biochemically histopathology. Results exhibited a marked increase levels, whereas isoform Treatment troglitazone or rosiglitazone resulted severe microvesicular periacinar steatosis, lean control did not develop any pathological changes. however, altered treatment. Conclusions In obesity-associated expression, thiazolidinediones may produce steatosis. Under pathophysiological conditions, such as non-insulin-dependent diabetes, thus become sensitized towards -activating drugs.