{"title":"News in brief","authors":"David Orme-Smith Bds","doi":"10.1586/eem.10.55","DOIUrl":null,"url":null,"abstract":"Published in the July issue of Cell, two new studies have revealed further details regarding the relationship between bone and blood sugar regulation, through signaling pathways that operate via insulin and osteocalcin, a hormone secreted exclusively by osteoblasts. Gerard Karsenty of Columbia University (NY, USA) has announced that his group has revealed “a key molecular link between bone remodeling and metabolism.” Their study has presented independent evidence for the crucial role of insulin in bone in regulating glucose via osteocalcin. Thomas Clemens of John Hopkins University School of Medicine (MD, USA) and colleagues were surprised by their observations after they engineered a mouse that lacked insulin receptors in their osteoblasts. “The mice started to get fat,” he said. They showed changes in their biochemistry that were consistent with insulin resistance. They also had low osteocalacin levels and fewer osteoblasts to produce less bone.” As the animals aged, developing more severe blood sugar problems, glucose intolerance and insulin resistance, their symptoms were seen to improve with osteocalcin treatment.” According to the researchers, mice whose bones were unable to respond to insulin developed high blood sugar levels as well as insulin resistance – classic symptoms of diabetes. However, these were found to be tied to a drop in osteocalcin levels. Both teams have suggested that their findings could point to osteocalacin, or an alternative drug that is able to target bone, potentially being able to provide a novel treatment in the fight against Type 2 diabetes.","PeriodicalId":8713,"journal":{"name":"BDJ","volume":"15 1","pages":"332-332"},"PeriodicalIF":0.0000,"publicationDate":"1967-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"BDJ","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1586/eem.10.55","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Published in the July issue of Cell, two new studies have revealed further details regarding the relationship between bone and blood sugar regulation, through signaling pathways that operate via insulin and osteocalcin, a hormone secreted exclusively by osteoblasts. Gerard Karsenty of Columbia University (NY, USA) has announced that his group has revealed “a key molecular link between bone remodeling and metabolism.” Their study has presented independent evidence for the crucial role of insulin in bone in regulating glucose via osteocalcin. Thomas Clemens of John Hopkins University School of Medicine (MD, USA) and colleagues were surprised by their observations after they engineered a mouse that lacked insulin receptors in their osteoblasts. “The mice started to get fat,” he said. They showed changes in their biochemistry that were consistent with insulin resistance. They also had low osteocalacin levels and fewer osteoblasts to produce less bone.” As the animals aged, developing more severe blood sugar problems, glucose intolerance and insulin resistance, their symptoms were seen to improve with osteocalcin treatment.” According to the researchers, mice whose bones were unable to respond to insulin developed high blood sugar levels as well as insulin resistance – classic symptoms of diabetes. However, these were found to be tied to a drop in osteocalcin levels. Both teams have suggested that their findings could point to osteocalacin, or an alternative drug that is able to target bone, potentially being able to provide a novel treatment in the fight against Type 2 diabetes.