Bone and joint neuropathy in rats with type-2 diabetes

Tashfeen Ahmad, Anna Ugarph-Morawski, Jian Li, Indre Bileviciute-Ljungar, Anja Finn, Claes Göran Östenson, Andris Kreicbergs

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)


We have previously demonstrated that Goto-Kakizaki (GK) rats with spontaneous type-2 diabetes and peripheral neuropathy exhibit regional osteopathic changes. In the present study on 18 GK rats and 21 control Wistar rats, the occurrence of the sensory neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP), and the autonomic neuropeptide Y (NPY) was analysed in bone and joints, dorsal root ganglia and lumbar spinal cord by immunohistochemistry and radioimmunoassay (RIA). Immunohistochemistry disclosed a predominance of immunoreactivities in vessel-related nerve fibers, although some were also seen in free terminals. While SP, CGRP and NPY in periosteum, cortical bone and synovium was confined to neuronal tissue, the bone marrow in addition exhibited an abundance of NPY-positive megakaryocytes. Apart from this cellular source of NPY, the observations suggest that the three neuropeptides analysed in bone and joints are of neuronal origin. Quantification by RIA showed a significant decrease of NPY in cortical bone (-36%), bone marrow (-66%) and ankle (-29%) of GK rats. CGRP was decreased in the spinal cord (-19%) and dorsal root ganglia (-26%) but was unchanged in bone and joints, as with SP. Given the suggested anabolic role of NPY and CGRP on bone, neuropeptidergic deficit in diabetes may prove to be an important factor underlying the development of regional osteopenia.

Original languageEnglish
Pages (from-to)61-67
Number of pages7
JournalRegulatory Peptides
Issue number1-2
Publication statusPublished - 15 Jun 2004
Externally publishedYes


  • Calcitonin gene-related peptide
  • Diabetic neuropathy
  • Diabetic osteopathy
  • Goto-Kakizaki rat
  • Neuropeptide Y
  • Neuropeptides
  • Substance P


Dive into the research topics of 'Bone and joint neuropathy in rats with type-2 diabetes'. Together they form a unique fingerprint.

Cite this