1998
DOI: 10.1016/s8756-3282(97)00220-2
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Growth-Inhibitory Effect of a High Glucose Concentration on Osteoblast-like Cells

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Cited by 171 publications
(114 citation statements)
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“…It is also unclear whether hyperglycemia has a role in maintaining normal bone mass in some cases of diabetes, and may protect against bone loss during early stages of the disease [9]. Although the role of glucose in osteoblast differentiation and mineralization has been examined [10][11][12][13][14], little is known regarding its effect on osteoclast differentiation and function. Our findings indicate that high D-Glc inhibits osteoclastogenesis, likely by preventing the formation of pre-osteoclast cells capable of fusing into multinucleated osteoclasts.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…It is also unclear whether hyperglycemia has a role in maintaining normal bone mass in some cases of diabetes, and may protect against bone loss during early stages of the disease [9]. Although the role of glucose in osteoblast differentiation and mineralization has been examined [10][11][12][13][14], little is known regarding its effect on osteoclast differentiation and function. Our findings indicate that high D-Glc inhibits osteoclastogenesis, likely by preventing the formation of pre-osteoclast cells capable of fusing into multinucleated osteoclasts.…”
Section: Discussionmentioning
confidence: 99%
“…Hyperglycemia has been implicated in the pathogenesis of diabetic bone disease and, decreased activity of osteoblasts under diabetic conditions has been reported in both animal models and humans [9,10]. In vitro, incubation of cultured osteoblast-like cells with high glucose inhibits mineralization, Insulinlike Growth Factor-I (IGF-I)-stimulated growth and modulates osteoblast gene expression [11][12][13][14]. Studies are conflicting as to whether osteoclastogenesis is altered in diabetes [6].…”
Section: Introductionmentioning
confidence: 99%
“…Several studies have demonstrated that type-2 diabetic osteoporosis is associated with depression of osteoblastic activities, resulting in a decrease in bone formation (Inaba et al 1999, Takizawa et al 2003. In in vitro studies, elevated extracellular glucose has been shown to change osteoblast phenotype by inhibiting osteocalcin expression (Inaba et al 1995, Terada et al 1998, Zayzafoon et al 2002. Irreversible advanced glycosylation end-products (AGEs) are generated by even sporadic elevations in blood glucose and appear to act through specific receptors (RAGEs) to increase the levels of inflammatory cytokines (tumor necrosis factor-α and interleukin-6), which have been shown to negatively affect the balance of bone formation/resorption.…”
Section: Discussionmentioning
confidence: 99%
“…On one hand, hyperinsulinemia and relatively high BMI are protective against bone loss in type 2 diabetes mellitus. On the other, increased calciuria and decreased osteoblastic function due to hyperglycemia may lead to deterioration of bone mass (Terada et al 1998). Considering the likelihood that patients with type 2 diabetes mellitus may potentially be at a somewhat higher risk of developing osteoporosis, treatment with TZDs could increase this risk further.…”
Section: Figurementioning
confidence: 99%