作者: G. Mabilleau , A. Mieczkowska , M. E. Edmonds
DOI: 10.1111/J.1464-5491.2010.03048.X
关键词: Thiazolidinedione 、 Rosiglitazone 、 Endocrinology 、 Medicine 、 RANKL 、 Osteocyte 、 Programmed cell death 、 Pioglitazone 、 Troglitazone 、 Sclerostin 、 Internal medicine
摘要: Diabet. Med. 27, 925–932 (2010) Abstract Aims Thiazolidinediones (TZDs) are associated with a higher risk of bone fracture in women compared men. The aim the present study was to investigate whether TZDs could influence osteocyte behaviour and contribute skeletal phenotype observed TZD-treated patients. Methods murine MLO-Y4 cell line used as source osteocytes. These cells were cultured for 24 h 0, 10−8 m, 10−7 m, 10−6 m, 10−5 m or 10−4 m pioglitazone, rosiglitazone troglitazone presence absence 17β-oestradiol. extent apoptosis assessed, expression formation inhibitor sclerostin receptor activator nuclear factor κB ligand (RANKL) also. Results In 17β-oestradiol, induced dose-dependently even at lowest concentration 10−8 m. Furthermore, but not RANKL significantly increased cultures untreated cultures. 17β-oestradiol reduced TZD-induced also up-regulation. Conclusions findings therefore raise potential concern using post-menopausal where lack oestrogen would prevent up-regulation may aggravate reduction mass these patients.