Commentary: Changes in bone biological markers after treatment of Iranian diabetic patients with pioglitazone: No relation to polymorphism of PPAR‑γ (Pro12Ala)

The article “Changes in bone biological markers after treatment of Iranian diabetic patients with pioglitazone: No relation to polymorphism of PPAR‑γ (Pro12Ala) that published in recent issue encourage us to think about changes of bone mineral density with commonly used drugs to control hyperglycemia in type 2 diabetic patients. Thiazolidinediones including pioglitazone are agents that lower blood glucose by improving target cell response to insulin. Pioglitazone is a selective agonist for peroxisome proliferator‑activated receptor‑gamma (PPAR‑γ). Activation of nuclear PPAR‑γ receptors influences the production of a number of gene products involved in glucose metabolism. There are also evidences that these drugs could affect the process of bone remodeling. In animal studies, PPAR‑γ agonist treatment was followed by increased bone loss and impaired osteoblast function. Few human studies evaluated the effects of treatment with PPAR agonist on BMD and measures of bone turnover. Activation of PPAR‑γ pathway by an endogenous PPAR‑γ ligand inhibited the formation and activation of osteoclasts in human mesenchymal stem cells.