ArticleCell chemical biology2023
Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes.
Article in Cell chemical biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 17 citations in OpenAlex.
- H3K18la in periodontal ligament fibroblasts regulates immune niches and alveolar bone remodeling under mechanical loads.International journal of oral science · 2026Article
- Glucose metabolism in osteoporosis: A potential therapeutic target (Review).International journal of molecular medicine · 2026Review
- Translational boundaries of Txnip-targeted metabolic modulation in bone homeostasis.Journal of orthopaedic translation · 2026Article
- Apoptosis of Mdm2-deficient osteocytes enhances osteogenesis through TRPM8-enriched apoptotic vesicles.Bone research · 2026Article
- Metabolic checkpoints in bone remodeling: from dysregulation to targeted therapies.Clinics (Sao Paulo, Brazil) · 2026Review
- Fgf18 marks reserve skeletal progenitors in the fibrous periosteum contributing to bone fracture repair.Cell reports · 2026Article
- Txnip regulates glycolysis and tricarboxylic acid cycle balance to maintain bone homeostasis.Journal of orthopaedic translation · 2026Article
- IGF-1 from bone marrow Adipoq-lineage cells stimulates endocortical bone formation in mature female mice.JBMR plus · 2026Article
- A single cell atlas defines perinatal factors that drive murine bone marrow development.bioRxiv : the preprint server for biology · 2026Article
- Trabecular-Like Scaffold Dictates Osteogenesis via Fluid Shear Stress-Induced Metabolic Reprogramming through the CAV1-HIF-1α Axis.Research (Washington, D.C.) · 2026Article
- Metabolic mediators linking type 1 diabetes mellitus to osteoporosis.Archives of medical science : AMS · 2026Article
- Fueling bone loss: the immunometabolic reprogramming of the bone microenvironment in diabetic osteoporosis.Frontiers in immunology · 2026Review
- An adipo-osteoprogenitor population in the endosteal niche contributes to bone and fat formation in adult mouse bone marrow.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- IGF-1 from bone marrow Adipoq-lineage cells stimulates endocortical bone formation in mature female mice.bioRxiv : the preprint server for biology · 2025Article
- Accelerated osteocytic citrate production in chronic kidney disease is associated with protection of the kidney.bioRxiv : the preprint server for biology · 2025Article
- Single-cell profiling reveals periosteal signatures of impaired periosteal cells proliferation in a drill-hole model of type 2 diabetes.Cell communication and signaling : CCS · 2025Article
- Roles of myokines in osteoporosis under physiological and diabetic conditions.Frontiers in endocrinology · 2025Review
- Metabolic reprogramming in skeletal cell differentiation.Bone research · 2024Review
- The multifaceted roles of mitochondria in osteoblasts: from energy production to mitochondrial-derived vesicle secretion.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Review
- Metabolic regulation of skeletal cell fate and function.Nature reviews. Endocrinology · 2024Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Type I diabetes (T1D) impairs bone accrual in patients, but the mechanism is unclear. Here in a murine monogenic model for T1D, we demonstrate that diabetes suppresses bone formation resulting in a rapid loss of both cortical and trabecular bone. Single-cell RNA sequencing uncovers metabolic dysregulation in bone marrow osteogenic cells of diabetic mice. In vivo stable isotope tracing reveals impaired glycolysis in diabetic bone that is highly responsive to insulin stimulation. Remarkably, deletion of the insulin receptor reduces cortical but not trabecular bone. Increasing glucose uptake by overexpressing Glut1 in osteoblasts exacerbates bone defects in T1D mice. Conversely, activation of glycolysis by Pfkfb3 overexpression preserves both trabecular and cortical bone mass in the face of diabetes. The study identifies defective glucose metabolism in osteoblasts as a pathogenic mechanism for osteopenia in T1D, and furthermore implicates boosting osteoblast glycolysis as a potential bone anabolic therapy.
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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.