Diabetes, TZDs, and Bone: A Review of the Clinical Evidence
Evidence from rodent and in vitro models suggests that activation of PPAR-γ by thiazolidinediones (TZDs) causes increased bone marrow adiposity and decreased osteoblastogenesis, resulting in bone loss. TZDs are prescribed for the treatment of diabetes, providing an opportunity to determine whether P...
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| Format: | Article |
| Language: | English |
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Wiley
2006-01-01
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| Series: | PPAR Research |
| Online Access: | http://dx.doi.org/10.1155/PPAR/2006/24502 |
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| _version_ | 1832552013913653248 |
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| author | Ann V. Schwartz |
| author_facet | Ann V. Schwartz |
| author_sort | Ann V. Schwartz |
| collection | DOAJ |
| description | Evidence from rodent and in vitro models suggests that activation of PPAR-γ by thiazolidinediones (TZDs) causes increased bone marrow adiposity and
decreased osteoblastogenesis, resulting in bone loss. TZDs are prescribed for
the treatment of diabetes, providing an opportunity to determine whether PPAR-γ activation also impacts bone in humans. In addition, since type 2 diabetes is
associated with higher fracture risk, an understanding of the clinical impact of
TZDs on bone is needed to guide fracture prevention efforts in this population.
This review summarizes current findings regarding type 2 diabetes and increased
fracture risk and then considers the available evidence regarding TZD use and
bone metabolism in humans. |
| format | Article |
| id | doaj-art-5d23f5ba9e074799bfa2bf367a9c942b |
| institution | Kabale University |
| issn | 1687-4757 1687-4765 |
| language | English |
| publishDate | 2006-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | PPAR Research |
| spelling | doaj-art-5d23f5ba9e074799bfa2bf367a9c942b2025-02-03T05:59:41ZengWileyPPAR Research1687-47571687-47652006-01-01200610.1155/PPAR/2006/2450224502Diabetes, TZDs, and Bone: A Review of the Clinical EvidenceAnn V. Schwartz0Department of Epidemiology and Biostatistics, University of California, San Francisco, 185 Berry Street, Suite 5700, San Francisco 94107, CA, USAEvidence from rodent and in vitro models suggests that activation of PPAR-γ by thiazolidinediones (TZDs) causes increased bone marrow adiposity and decreased osteoblastogenesis, resulting in bone loss. TZDs are prescribed for the treatment of diabetes, providing an opportunity to determine whether PPAR-γ activation also impacts bone in humans. In addition, since type 2 diabetes is associated with higher fracture risk, an understanding of the clinical impact of TZDs on bone is needed to guide fracture prevention efforts in this population. This review summarizes current findings regarding type 2 diabetes and increased fracture risk and then considers the available evidence regarding TZD use and bone metabolism in humans.http://dx.doi.org/10.1155/PPAR/2006/24502 |
| spellingShingle | Ann V. Schwartz Diabetes, TZDs, and Bone: A Review of the Clinical Evidence PPAR Research |
| title | Diabetes, TZDs, and Bone: A Review of the Clinical Evidence |
| title_full | Diabetes, TZDs, and Bone: A Review of the Clinical Evidence |
| title_fullStr | Diabetes, TZDs, and Bone: A Review of the Clinical Evidence |
| title_full_unstemmed | Diabetes, TZDs, and Bone: A Review of the Clinical Evidence |
| title_short | Diabetes, TZDs, and Bone: A Review of the Clinical Evidence |
| title_sort | diabetes tzds and bone a review of the clinical evidence |
| url | http://dx.doi.org/10.1155/PPAR/2006/24502 |
| work_keys_str_mv | AT annvschwartz diabetestzdsandboneareviewoftheclinicalevidence |