Original Research ARTICLE
Dapagliflozin prevent osteoporosis in ZDF rats via alleviating hypercalciuria
- 1Department of Endocinology, Zhujiang Hospital, Southern Medical University, China
- 2Second Affiliated Hospital of Guizhou Medical University, China
Recent studies showed that SGLT2I (Sodium-dependent glucose transporters 2 inhibitor) may possess potential adverse effect on skeleton when treating type 2 diabetes mellitus (T2DM). However, whether SGLT2I aggravates osteoporosis in patients with T2DM and the particular mechanism remains controversial. In this study, we explored whether the usage of Dapagliflozin alleviated diabetic related osteoporosis in animal models. The effect of Dapagliflozin on skeleton was evaluated in male ZDF (Zucker Diabetic Fatty) rats -a rat model of diet induced spontaneous T2DM, and Dapagliflozin were administrated via gavage. Skeleton tissue mineral density and microarchitecture were measured along with serum bone biomarkers and other metabolic parameters. We found decreased cortical bone mass density after SGLT2I treatment while trabecular bone mass density and ductility received a rise. These changes in bone morphology were possibly connected to the change in hyperglycemia and ion metabolism caused by calcitonin. Our results indicating that SGLT2I may help to prevent the skeleton damage caused by diabetes. The aggravation of diabetic related osteoporosis and increased factures demonstrated by the recent clinical researches were probably the outcome of the holistic changes in diabetic individuals after administrated SGLT2I.
Keywords: dapagliflozin, ZDF rats, type 2 diabetes mellitus, SGLT-2i, bone microarchitecture
Received: 05 May 2019;
Accepted: 27 Sep 2019.
Copyright: © 2019 Wang, Cheng, Yang, An, Chen, Zhang and Yang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Mx. Hong Chen, Department of Endocinology, Zhujiang Hospital, Southern Medical University, Guang Zhou, China, email@example.com
Mx. Hua Zhang, Department of Endocinology, Zhujiang Hospital, Southern Medical University, Guang Zhou, China, firstname.lastname@example.org
Mx. Li Yang, Department of Endocinology, Zhujiang Hospital, Southern Medical University, Guang Zhou, China, email@example.com