Insulin does not rescue cortical and trabecular bone loss in type 2 diabetic Goto-Kakizaki rats

• Main Authors: Ratchaneevan Aeimlapa, Narattaphol Charoenphandhu, Panan Suntornsaratoon, Kannikar Wongdee, Wacharaporn Tiyasatkulkovit, Kanchana Kengkoom, Nateetip Krishnamra
• Other Authors: Chulalongkorn University
• Format: Article
• Published: 2019
• Subjects: Biochemistry, Genetics and Molecular Biology
• Online Access: https://repository.li.mahidol.ac.th/handle/123456789/45059
• Institution: Mahidol University

© 2017, The Physiological Society of Japan and Springer Japan KK. In type 2 diabetes mellitus (T2DM), the decreased bone strength is often associated with hyperglycemia and bone cell insulin resistance. Since T2DM is increasingly reported in young adults, it is not known whether the effect of T2DM on bone would be different in young adolescents and aging adults. Here, we found shorter femoral and tibial lengths in 7-month, but not 13-month, Goto-Kakizaki (GK) T2DM rats as compared to wild-type rats. Bone µCT analysis showed long-lasting impairment of both cortical and trabecular bones in GK rats. Although insulin treatment effectively improved hyperglycemia, it was not able to rescue trabecular BMD and cortical thickness in young adult GK rats. In conclusion, insulin treatment and alleviation of hyperglycemia did not increase BMD of osteopenic GK rats. It is likely that early prevention of insulin resistance should prevail over treatment of full-blown T2DM-related osteopathy.