ArticleEndocrinology2013
GSK-3β function in bone regulates skeletal development, whole-body metabolism, and male life span.
Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Gastric bypass surgery with exercise alters plasma microRNAs that predict improvements in cardiometabolic risk.International journal of obesity (2005) · 2017Trial
- Low-dose lithium supplementation promotes musculoskeletal and metabolic health in ovariectomized female mice.The Journal of physiology · 2026Article
- Induction of osteogenic differentiation of MSCs by GSK3β knockdown through GSK3β siRNAs transfection.PloS one · 2026Article
- The crucial role of beta-catenin in the osteoprotective effect of semaglutide in an ovariectomized rat model of osteoporosis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- GSK3 inhibition improves skeletal muscle function and whole-body metabolism in male mouse models of Duchenne muscular dystrophy.Nature communications · 2024Article
- Article
- The skeleton: an overlooked regulator of systemic glucose metabolism in cancer?Frontiers in oncology · 2024Article
- GSK-3 at the heart of cardiometabolic diseases: Isoform-specific targeting is critical to therapeutic benefit.Biochimica et biophysica acta. Molecular basis of disease · 2023Review
- Article
- Novel Therapeutic Targets for Fibrodysplasia Ossificans Progressiva: Emerging Strategies and Future Directions.Cureus · 2023Review
- Glycogen synthase kinase 3 alpha/beta deletion induces precocious growth plate remodeling in mice.Journal of molecular medicine (Berlin, Germany) · 2021Article
- The mTORC1 complex in pre-osteoblasts regulates whole-body energy metabolism independently of osteocalcin.Bone research · 2021Article
- Article
- Silencing of lncRNAInternational journal of molecular sciences · 2019Article
- The role of osteoblasts in energy homeostasis.Nature reviews. Endocrinology · 2019Review
- Podocyte GSK3 is an evolutionarily conserved critical regulator of kidney function.Nature communications · 2019Article
- Vhl deletion in osteoblasts boosts cellular glycolysis and improves global glucose metabolism.The Journal of clinical investigation · 2018Article
- Bone Cell Bioenergetics and Skeletal Energy Homeostasis.Physiological reviews · 2017Review
- Frontal Bone Insufficiency in Gsk3β Mutant Mice.PloS one · 2016Article
- DKK1 is a potential novel mediator of cisplatin-refractoriness in non-small cell lung cancer cell lines.BMC cancer · 2015Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
Abstract
Glycogen synthase kinase 3 β (GSK-3β) is an essential negative regulator or "brake" on many anabolic-signaling pathways including Wnt and insulin. Global deletion of GSK-3β results in perinatal lethality and various skeletal defects. The goal of our research was to determine GSK-3β cell-autonomous effects and postnatal roles in the skeleton. We used the 3.6-kb Col1a1 promoter to inactivate the Gsk3b gene (Col1a1-Gsk3b knockout) in skeletal cells. Mutant mice exhibit decreased body fat and postnatal bone growth, as well as delayed development of several skeletal elements. Surprisingly, the mutant mice display decreased circulating glucose and insulin levels despite normal expression of GSK-3β in metabolic tissues. We showed that these effects are due to an increase in global insulin sensitivity. Most of the male mutant mice died after weaning. Prior to death, blood glucose changed from low to high, suggesting a possible switch from insulin sensitivity to resistance. These male mice die with extremely large bladders that are preceded by damage to the urogenital tract, defects that are also seen type 2 diabetes. Our data suggest that skeletal-specific deletion of GSK-3β affects global metabolism and sensitizes male mice to developing type 2 diabetes.
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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.