ArticleScientific reports2019
Elevated glucose acts directly on osteocytes to increase sclerostin expression in diabetes.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Bone Morphogenetic Proteins in Obesity Management: Therapeutic Potential and Challenges Beyond the Skeleton.Current medical science · 2026Review
- Type 2 Diabetes Modulates Mesenchymal Stem Cell Response to Advanced Glycation End Products and N-Acetylcysteine Antioxidant Effect.Pharmaceutics · 2026Article
- Bone Organoids: A Novel Tool for Modeling and Managing Skeletal Disorders in Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Severe Osteoporosis in a Young Woman With Type 1 Diabetes and Pancreatic Exocrine Insufficiency.Case reports in endocrinology · 2026Article
- Association of total and bioactive serum sclerostin levels with bone metabolism in type 2 diabetes mellitus.Journal of clinical & translational endocrinology · 2025Article
- Effect of High Glucose and Carboxymethyl-Lysine on Osteocyte Gene Expression.American journal of molecular biology · 2025Article
- Risk factors for osteoporosis in elderly patients with type 2 diabetes: A protocol for systematic review and meta-analysis.PloS one · 2025Article
- Localized sclerostin accumulation in osteocyte lacunar-canalicular system is associated with cortical bone microstructural alterations and bone fragility inFrontiers in cell and developmental biology · 2025Article
- Article
- Short- and long-term exposure to high glucose induces unique transcriptional changes in osteoblasts in vitro.Biology open · 2024Article
- Close negative correlation of local and circulating Dickkopf-1 and Sclerostin levels during human fracture healing.Scientific reports · 2024Article
- Evaluating the correlation of sclerostin levels with obesity and type 2 diabetes in a multiethnic population living in Kuwait.Frontiers in endocrinology · 2024Article
- Microvascular Disease Associates with Larger Osteocyte Lacunae in Cortical Bone in Type 2 Diabetes Mellitus.JBMR plus · 2023Article
- Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating sclerostin expression.iScience · 2023Article
- Regulation of the Osteocyte Secretome with Aging and Disease.Calcified tissue international · 2023Review
- Biochemical Markers of Bone Fragility in Patients with DiabetesThe Journal of clinical endocrinology and metabolism · 2023Article
- The role of wnt signaling in diabetes-induced osteoporosis.Diabetology & metabolic syndrome · 2023Review
- In-Vitro Evaluation of Photofunctionalized Implant Surfaces in a High-Glucose Microenvironment Simulating Diabetics.Journal of functional biomaterials · 2023Article
- Endocrine Functions of Sclerostin.Current opinion in endocrine and metabolic research · 2023Article
- Iron metabolism and ferroptosis in diabetic bone loss: from mechanism to therapy.Frontiers in nutrition · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Bone quality in diabetic patients is compromised, leading to weaker bones and increased fracture risk. However, the mechanism by which this occurs in diabetic bone remains to be fully elucidated. We hypothesized that elevated glucose and glucose variation would affect the function of osteocytes, essential regulators of bone homeostasis and quality. To first test this hypothesis, we used the IDG-SW3 osteocyte-like cell line to examine the effects of glucose levels on osteocyte function and viability in vitro. We confirmed our in vitro findings using the in vivo streptozotocin-induced (STZ) diabetic rat model and ex-vivo cultured osteocytes from these rats. IDG-SW3 cells cultured under high glucose conditions displayed significantly increased Sost mRNA(100-fold) and sclerostin protein, a negative regulator of bone formation(5000-fold), compared to cells in control media. mRNA expression of osteoblast markers such as Osx, Ocn and Col1a1 was unaffected by glucose. Factors associated with osteoclast activation were affected by glucose, with Rankl being upregulated by low glucose. Opg was also transiently upregulated by high glucose in mature IDG-SW3 cells. Induction of diabetes in Sprague-Dawley rats via a single dose of STZ (70 mg/kg) resulted in elevated maximum glucose and increased variability compared to control animals (670/796 vs. 102/142 mg/dL). This was accompanied by increased Sost/sclerostin expression in the osteocytes of these animals. These results show that glucose levels directly regulate osteocyte function through sclerostin expression and suggest a potential mechanism for the negative impact of diabetes on bone quality.
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