ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2015
An insulin-sensitizing thiazolidinedione, which minimally activates PPARγ, does not cause bone loss.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 44 citations in OpenAlex.
- Adipocyte Hyperplasia Facilitated Adipose Tissue Expansion to Alleviate Hepatopancreas Injury in Nile Tilapia (Aquaculture nutrition · 2025Article
- β-Sitosterol Reduces the Content of Triglyceride and Cholesterol in a High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease Zebrafish (Animals : an open access journal from MDPI · 2024Article
- The role of TRPV2 as a regulator on the osteoclast differentiation during orthodontic tooth movement in rats.Scientific reports · 2023Article
- Pharmacotherapy for Non-Alcoholic Fatty Liver Disease: Emerging Targets and Drug Candidates.Biomedicines · 2022Review
- The pathophysiology of osteoporosis in obesity and type 2 diabetes in aging women and men: The mechanisms and roles of increased bone marrow adiposity.Frontiers in endocrinology · 2022Review
- Preliminary Phytochemical Screening, In Vitro Antidiabetic, Antioxidant Activities, and Toxicity of Leaf Extracts ofPlants (Basel, Switzerland) · 2021Article
- Article
- Increased marrow adipogenesis does not contribute to age-dependent appendicular bone loss in female mice.Aging cell · 2020Article
- Oral Nano Drug Delivery Systems for the Treatment of Type 2 Diabetes Mellitus: An Available Administration Strategy for Antidiabetic Phytocompounds.International journal of nanomedicine · 2020Review
- Rosiglitazone suppresses RANKL-induced NFATc1 autoamplification by disrupting the physical interaction between NFATc1 and PPARγ.FEBS open bio · 2018Article
- CMHX008, a PPARγ partial agonist, enhances insulin sensitivity with minor influences on bone loss.Genes & diseases · 2018Article
- Advances and challenges in the management of advanced fibrosis in nonalcoholic steatohepatitis.Therapeutic advances in gastroenterology · 2018Review
- Obesity and nonalcoholic fatty liver disease: current perspectives.Diabetes, metabolic syndrome and obesity : targets and therapy · 2018Review
- Effects of Lobeglitazone, a New Thiazolidinedione, on Osteoblastogenesis and Bone Mineral Density in Mice.Endocrinology and metabolism (Seoul, Korea) · 2017Article
- PPAR-γ regulates pharmacological but not physiological or pathological osteoclast formation.Nature medicine · 2016Article
- ASXL2 Regulates Glucose, Lipid, and Skeletal Homeostasis.Cell reports · 2015Article
- Novel insulin sensitizer MSDC-0602K improves insulinemia and fatty liver disease in mice, alone and in combination with liraglutide.The Journal of biological chemistryArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Rosiglitazone is an insulin-sensitizing thiazolidinedione (TZD) that activates the transcription factor peroxisome proliferator-activated receptor gamma (PPARγ). Although rosiglitazone effectively treats type II diabetes mellitus (T2DM), it carries substantial complications, including increased fracture risk. This predisposition to fracture is consistent with the fact that PPARγ preferentially promotes formation of adipocytes at the cost of osteoblasts. Rosiglitazone-activated PPARγ, however, also stimulates osteoclast formation. A new TZD analog with low affinity for binding and activation of PPARγ but whose insulin-sensitizing properties mirror those of rosiglitazone has been recently developed. Because of its therapeutic implications, we investigated the effects of this new TZD analog (MSDC-0602) on skeletal homeostasis, in vitro and in vivo. Confirming it activates the nuclear receptor in osteoclasts, rosiglitazone enhances expression of the PPARγ target gene, CD36. MSDC-0602, in contrast, minimally activates PPARγ and does not alter CD36 expression in the bone-resorptive cells. Consistent with this finding, rosiglitazone increases receptor activator of NF-κB ligand (RANKL)-induced osteoclast differentiation and number, whereas MSDC-0602 fails to do so. To determine if this new TZD analog is bone sparing, in vivo, we fed adult male C57BL/6 mice MSDC-0602 or rosiglitazone. Six months of a rosiglitazone diet results in a 35% decrease in bone mass with increased number of osteoclasts, whereas that of MSDC-0602-fed mice is indistinguishable from control. Thus, PPARγ sparing eliminates the skeletal side effects of TZDs while maintaining their insulin-sensitizing properties.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.