| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2048064 | FEBS Letters | 2013 | 6 Pages |
Doxorubicin-treated animals show elevated serum triglyceride and blood glucose levels. Adipocytes play an important role in buffering blood glucose and lipids. A raise in serum lipid level triggers adipogenesis in order to increase the lipid absorption capacity of adipose tissue. Doxorubicin inhibits adipogenesis through the down-regulation of PPARγ, a crucial component of the lipid metabolic pathway which controls the expression of glucose and fatty acid transporters. Doxorubicin-mediated down-regulation of PPARγ inhibits blood glucose and lipid clearance thereby causing hyperglycemia and hyperlipidemia resulting in lipotoxicity, glucotoxicity, inflammation and insulin resistance. Therefore we hypothesize that doxorubicin treatment could mimic a type 2 diabetic condition.
► Doxorubicin down-regulates PPARγ, may subsequently affect the expression of GLUT4 & FAT/CD36. ► Reduction of glucose and fatty acid transporters would cause hyperglycemia and hyperlipidemia. ► Free fatty acids induced inflammation of adipose tissue leads to insulin resistance. ► Inflamed adipose tissue confers to type 2 diabetes like condition in doxorubicin treated animals.
