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首页> 外文期刊>Journal of Cellular Physiology >Inhibition of PPARgamma prevents type I diabetic bone marrow adiposity but not bone loss.
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Inhibition of PPARgamma prevents type I diabetic bone marrow adiposity but not bone loss.

机译：抑制PPARgamma防止I型糖尿病骨髓脂肪过多而不是骨质流失。

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Diabetes type I is associated with bone loss and increased bone adiposity. Osteoblasts and adipocytes are both derived from mesenchymal stem cells located in the bone marrow, therefore we hypothesized that if we could block adipocyte differentiation we might prevent bone loss in diabetic mice. Control and insulin-deficient diabetic BALB/c mice were chronically treated with a peroxisomal proliferator-activated receptor gamma (PPARgamma) antagonist, bisphenol-A-diglycidyl ether (BADGE), to block adipocyte differentiation. Effects on bone density, adiposity, and gene expression were measured. BADGE treatment did not prevent diabetes-associated hyperglycemia or weight loss, but did prevent diabetes-induced hyperlipidemia and effectively blocked diabetes type I-induced bone adiposity. Despite this, BADGE treatment did not prevent diabetes type I suppression of osteoblast markers (runx2 and osteocalcin) and bone loss (as determined by micro-computed tomography). BADGE did not suppress osteoblast gene expression or bone mineral density in control mice, however, chronic (but not acute) BADGE treatment did suppress osteocalcin expression in osteoblasts in vitro. Taken together, our findings suggest that BADGE treatment is an effective approach to reduce serum triglyceride and free fatty acid levels as well as bone adiposity associated with type I diabetes. The inability of BADGE treatment to prevent bone loss in diabetic mice suggests that marrow adiposity is not linked to bone density status in type I diabetes, but we cannot exclude the possibility of additional BADGE effects on osteoblasts or other bone cells, which could contribute to preventing the rescue of the bone phenotype.
机译：I型糖尿病与骨质疏松和相关联增加骨肥胖。脂肪细胞都来源于间充质干细胞细胞位于骨髓,因此我们假设,如果我们能阻止脂肪细胞分化我们可能防止骨质流失糖尿病小鼠。糖尿病BALB / c小鼠长期治疗与过氧化物酶病proliferator-activated受体γ(PPARgamma)拮抗剂,bisphenol-A-diglycidyl醚(徽章),阻止脂肪细胞的分化。密度、肥胖和基因表达测量。糖尿病危害高血糖或减肥,但防止diabetes-induced高脂血症,有效地阻止了我诱导型糖尿病骨肥胖。不能阻止糖尿病I型抑制成骨细胞标记(runx2和骨钙素)骨质疏松(如由微型电脑断层扫描)。基因表达或骨矿物质密度控制老鼠,然而,慢性(但不严重)徽章并抑制骨钙素治疗在成骨细胞在体外表达。在一起,我们的研究表明,徽章治疗是一种有效的方法来减少血清甘油三酯和游离脂肪酸水平以及骨与I型肥胖相关糖尿病防止糖尿病小鼠表明骨质流失骨髓脂肪过多与骨质密度无关在I型糖尿病状态,但我们不能排除额外的徽章的影响的可能性成骨细胞或其他骨骼细胞,这可能有助于防止骨的救援表现型。

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