Carla Ramírez Ruiz, Nerea Varo Cenarruzabeitia, Miriam Martínez Villanueva, Antonio M. Hernández Martínez, José Antonio Noguera Velasco
{"title":"Osteocalcin associates with bone mineral density and <i>VDR</i> gene polymorphisms in type 1 and type 2 diabetes","authors":"Carla Ramírez Ruiz, Nerea Varo Cenarruzabeitia, Miriam Martínez Villanueva, Antonio M. Hernández Martínez, José Antonio Noguera Velasco","doi":"10.1515/almed-2023-0131","DOIUrl":null,"url":null,"abstract":"Abstract Objectives Bone metabolism is impaired in diabetes mellitus (DM). Our objective is to evaluate the association of bone turnover markers (BTM) and vitamin D receptor ( VDR ) gene polymorphisms with bone mineral density (BMD) in DM type 1 (T1D) and DM type 2 (T2D). Methods 165 patients (53 T1D and 112 T2D) were enrolled. BMD was measured by dual-energy X-ray absorptiometry (DEXA). Plasma osteocalcin (OC), beta-CrossLaps (β-CTX) and N‐amino terminal propeptide of type I collagen (P1NP) and VDR gene polymorphisms were evaluated. Results Participants were 53 T1D (41 years [31–48]) and 112 T2D (60 years [51–66]). BMD were not statistically different between the groups. OC (p<0.001) and P1NP levels (p<0.001) were higher in patients with T1D. The areas under the curve for the prediction of bone pathology were 0.732 (p=0.038) for OC in T1D and 0.697 (p=0.007) in T2D. A significant association was found between lower lumbar BMD and the A allele of BsmI (p=0.03), the A allele of ApaI (p=0.04) and the allele C of the Taql (p=0.046). Also, a significant correlation was found with higher OC levels and the G allele of BsmI (p=0.044), C allele of ApaI (p=0.011), T allele of Taql (p=0.006) and with C allele of FokI (p=0.004). Conclusions The high negative predictive value of the cut-off point for OC suggests that could be useful in excluding the risk suffering bone loss, allowing offering a personalized clinical approach to prevent this pathology.","PeriodicalId":72097,"journal":{"name":"Advances in laboratory medicine","volume":"39 1","pages":"0"},"PeriodicalIF":1.1000,"publicationDate":"2023-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in laboratory medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1515/almed-2023-0131","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MEDICAL LABORATORY TECHNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Abstract Objectives Bone metabolism is impaired in diabetes mellitus (DM). Our objective is to evaluate the association of bone turnover markers (BTM) and vitamin D receptor ( VDR ) gene polymorphisms with bone mineral density (BMD) in DM type 1 (T1D) and DM type 2 (T2D). Methods 165 patients (53 T1D and 112 T2D) were enrolled. BMD was measured by dual-energy X-ray absorptiometry (DEXA). Plasma osteocalcin (OC), beta-CrossLaps (β-CTX) and N‐amino terminal propeptide of type I collagen (P1NP) and VDR gene polymorphisms were evaluated. Results Participants were 53 T1D (41 years [31–48]) and 112 T2D (60 years [51–66]). BMD were not statistically different between the groups. OC (p<0.001) and P1NP levels (p<0.001) were higher in patients with T1D. The areas under the curve for the prediction of bone pathology were 0.732 (p=0.038) for OC in T1D and 0.697 (p=0.007) in T2D. A significant association was found between lower lumbar BMD and the A allele of BsmI (p=0.03), the A allele of ApaI (p=0.04) and the allele C of the Taql (p=0.046). Also, a significant correlation was found with higher OC levels and the G allele of BsmI (p=0.044), C allele of ApaI (p=0.011), T allele of Taql (p=0.006) and with C allele of FokI (p=0.004). Conclusions The high negative predictive value of the cut-off point for OC suggests that could be useful in excluding the risk suffering bone loss, allowing offering a personalized clinical approach to prevent this pathology.