Thiazolidinediones on PPARγ: The Roles in Bone Remodeling
Author(s) -
Wei Wei,
Yihong Wan
Publication year - 2011
Publication title -
ppar research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 49
eISSN - 1687-4765
pISSN - 1687-4757
DOI - 10.1155/2011/867180
Subject(s) - rosiglitazone , bone remodeling , osteoblast , osteoclast , bone resorption , endocrinology , medicine , glucose homeostasis , peroxisome proliferator activated receptor , thiazolidinedione , osteoporosis , receptor , chemistry , diabetes mellitus , type 2 diabetes , insulin resistance , in vitro , biochemistry
Thiazolidinediones (TZDs) are synthetic PPAR γ (peroxisome proliferator-activated receptor gamma) agonists and a class of drugs for diabetes mellitus type 2 that can decrease blood sugar efficiently by enhancing insulin sensitivity. However, increased bone fracture risk in diabetic individuals treated with TZDs is one of the reported side effects. Recent studies show that TZDs such as rosiglitazone simultaneously inhibit osteoblast differentiation and activate osteoclast differentiation, leading to bone loss due to decreased bone formation and increased bone resorption. Furthermore, TZDs may activate PPAR γ in tissues other than bone, such as the hypothalamus-pituitary-gonad (HPG) axis to indirectly regulate bone mass. This paper will focus on current new developments that implicate potential mechanisms for how PPAR γ modulates skeletal homeostasis and how TZDs exert bone-loss side effects.
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