ArticleInternational journal of molecular sciences2015
High insulin levels in KK-Ay diabetic mice cause increased cortical bone mass and impaired trabecular micro-structure.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- A Review of the Relationship Between Insulin and Bone Health.Biomedicines · 2025Review
- Metabolic and Skeletal Characterization of the KK/ACalcified tissue international · 2024Article
- Progress in experimental models to investigate the in vivo and in vitro antidiabetic activity of drugs.Animal models and experimental medicine · 2024Review
- Insights and implications of sexual dimorphism in osteoporosis.Bone research · 2024Review
- Role of oxidative stress in impaired type II diabetic bone repair: scope for antioxidant therapy intervention?Frontiers in dental medicine · 2024Review
- Energy Metabolism and Ketogenic Diets: What about the Skeletal Health? A Narrative Review and a Prospective Vision for Planning Clinical Trials on this Issue.International journal of molecular sciences · 2021Review
- Uncarboxylated osteocalcin ameliorates hepatic glucose and lipid metabolism in KKAy mice via activating insulin signaling pathway.Acta pharmacologica Sinica · 2020Article
- Article
- Pathophysiology and Management of Type 2 Diabetes Mellitus Bone Fragility.Journal of diabetes research · 2020Review
- Effects of Diabetes on Bone Material Properties.Current osteoporosis reports · 2019Review
- Characteristics of bone strength and metabolism in type 2 diabetic model Tsumura, Suzuki, Obese Diabetes mice.Bone reports · 2018Article
- Low bone toughness in the TallyHO model of juvenile type 2 diabetes does not worsen with age.Bone · 2018Article
- Bone Tissue Collagen Maturity and Mineral Content Increase With Sustained Hyperglycemia in the KK-Ay Murine Model of Type 2 Diabetes.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018Article
- Changes in bone macro- and microstructure in diabetic obese mice revealed by high resolution microfocus X-ray computed tomography.Scientific reports · 2016Article
- Bradykinin receptors and EphB2/EphrinB2 pathway in response to high glucose-induced osteoblast dysfunction and hyperglycemia-induced bone deterioration in mice.International journal of molecular medicine · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes mellitus (T2DM) is a chronic disease characterized by hyperglycemia, hyperinsulinemia and complications, including obesity and osteoporosis. Rodents have been widely used to model human T2DM and investigate its effect on the skeleton. We aimed to investigate skeletal alterations in Yellow Kuo Kondo (KK-Ay) diabetic mice displaying high insulin and glucose levels. Bone mineral density (BMD), micro-architecture and bone metabolism-related genes were analyzed. The total femoral areal BMD (aBMD), cortical volumetric BMD (vBMD) and thickness were significantly increased in KK-Ay mice, while the trabecular vBMD and mineralized bone volume/tissue volume (BV/TV), trabecular thickness and number were decreased compared to C57BL mice. The expression of both osteoblast-related genes, such as osteocalcin (OC), bone sialoprotein, Type I Collagen, osteonectin, RUNX2 and OSX, and osteoclast-related genes, such as TRAP and TCIRG, were up-regulated in KK-Ay mice. Correlation analyses showed that serum insulin levels were positively associated with aBMD, cortical vBMD and thickness and negatively associated with trabecular vBMD and micro-architecture. In addition, serum insulin levels were positively related to osteoblast-related and osteoclast-related gene expression. Our data suggest that high insulin levels in KK-Ay diabetic mice may increase cortical bone mass and impair trabecular micro-structure by up-regulating osteoblast-and osteoclast-related gene expression.
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