Increase of peroxisome proliferator-activated receptor δ gene expression in the lungs of streptozotocin-induced diabetic rats

Peroxisome proliferator-activated receptors (PPARs) play key roles in the regulation of energy homeostasis and inflammation while the agonists of PPARα and PPARγ are recently used for therapy in clinic. However, functions of PPARδ are still unclear. In the present study, we investigated the changes of PPARδ gene expression in the lung of diabetic rats. The mean level of mRNA transcripts encoding PPARδ was increased in the lung isolated from streptozotocin-induced diabetic rats (STZ-diabetic rats) to about 1.6-fold of that in normal rats. Exogenous insulin at the dose sufficient to normalize the plasma glucose of STZ-diabetic rats reversed the mRNA level of PPARδ in lungs after a 4-day treatment. Similar results were also observed in STZ-diabetic rats that received the treatment of phlorizin to reverse the plasma glucose level for 4 days. Otherwise, the protein level of PPARδ was higher in the lung of STZ-diabetic rats than that in normal rats. Treatment with exogenous insulin or phlorizin reversed this elevated protein level of PPARδ in the lung of STZ-diabetic rats to near the normal level. The obtained results suggest that increase of plasma glucose is responsible for the higher gene expression of PPARδ in the lung of STZ-diabetic rats.