Diabetoporosis: Role of nitric oxide

Authors

  • Nasibeh Yousefzadeh Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran https://orcid.org/0000-0001-8592-2124
  • Sajad Jeddi Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran https://orcid.org/0000-0002-3911-6620
  • Khosrow Kashfi Department of Molecular, Cellular and Biomedical Sciences, City University of New York School of Medicine, New York, NY 10031, USA. Tel: +1 212-650-6641, E-mail: Kashfi@med.cuny.edu https://orcid.org/0000-0002-4060-7283
  • Asghar Ghasemi Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, No. 24, Parvaneh Street, Velenjak, P.O. Box: 19395-4763, Tehran, Iran. E-mail: Ghasemi@endocrine.ac.ir https://orcid.org/0000-0001-6867-2151

DOI:

https://doi.org/10.17179/excli2021-3541

Keywords:

diabetoporosis, nitric oxide

Abstract

Diabetoporosis, diabetic-related decreased bone quality and quantity, is one of the leading causes of osteoporotic fractures in subjects with type 2 diabetes (T2D). This is associated with lower trabecular and cortical bone quality, lower bone turnover rates, lower rates of bone healing, and abnormal posttranslational modifications of collagen. Decreased nitric oxide (NO) bioavailability has been reported within the bones of T2D patients and can be considered as one of the primary mechanisms by which diabetoporosis is manifested. NO donors increase trabecular and cortical bone quality, increase the rate of bone formation, accelerate the bone healing process, delay osteoporosis, and decrease osteoporotic fractures in T2D patients, suggesting the potential therapeutic implication of NO-based interventions. NO is produced in the osteoblast and osteoclast cells by three isoforms of NO synthase (NOS) enzymes. In this review, the roles of NO in bone remodeling in the normal and diabetic states are discussed. Also, the favorable effects of low physiological levels of NO produced by endothelial NOS (eNOS) versus detrimental effects of high pathological levels of NO produced by inducible NOS (iNOS) in diabetoporosis are summarized. Available data indicates decreased bone NO bioavailability in T2D and decreased expression of eNOS, and increased expression and activity of iNOS. NO donors can be considered novel therapeutic agents in diabetoporosis.

Published

2021-04-16

How to Cite

Yousefzadeh, N. ., Jeddi, S., Kashfi, K. ., & Ghasemi, A. (2021). Diabetoporosis: Role of nitric oxide . EXCLI Journal, 20, 764–780. https://doi.org/10.17179/excli2021-3541

Issue

Section

Review articles