Deficiency of glucagon gene-derived peptides induces peripheral polyneuropathy in mice
| Autor: | Saeko Asano, Yoshiaki Morishita, Hideki Kamiya, Yusuke Seino, Jiro Nakamura, Tatsuhito Himeno, Yoshiro Kato, Emiri Miura-Yura, Shin Tsunekawa, Mikio Motegi, Hiromi Nakai-Shimoda, Keiko Naruse, Masaki Kondo, Norio Ozeki, Sachiko Sasajima, Yusuke Hayashi, Emi Asano-Hayami, Yoshitaka Hayashi, Koichi Kato, Rieko Inoue, Makoto Kato, Mohammad Sarif Mohiuddin |
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| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Neurite Neuronal Outgrowth Glucagon-Like Peptides Neural Conduction Biophysics Nerve fiber Nerve Fibers Myelinated Biochemistry Glucagon Neuroprotection Mice 03 medical and health sciences 0302 clinical medicine Diabetic Neuropathies Glucagon-Like Peptide 1 Ganglia Spinal Internal medicine Receptors Glucagon Animals Medicine RNA Messenger Molecular Biology Pathological Mice Knockout Hypoalgesia business.industry Cell Biology medicine.disease Mice Inbred C57BL Disease Models Animal 030104 developmental biology Peripheral neuropathy medicine.anatomical_structure Endocrinology Hyperalgesia 030220 oncology & carcinogenesis Peripheral nervous system business |
| Zdroj: | Biochemical and Biophysical Research Communications. 532:47-53 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2020.08.007 |
| Popis: | Although diabetic polyneuropathy (DPN) is the commonest diabetic complication, its pathology remains to be clarified. As previous papers have suggested the neuroprotective effects of glucagon-like peptide-1 in DPN, the current study investigated the physiological indispensability of glucagon gene-derived peptides (GCGDPs) including glucagon-like peptide-1 in the peripheral nervous system (PNS). Neurological functions and neuropathological changes of GCGDP deficient (gcg−/−) mice were examined. The gcg−/− mice showed tactile allodynia and thermal hyperalgesia at 12–18 weeks old, followed by tactile and thermal hypoalgesia at 36 weeks old. Nerve conduction studies revealed a decrease in sensory nerve conduction velocity at 36 weeks old. Pathological findings showed a decrease in intraepidermal nerve fiber densities. Electron microscopy revealed a decrease in circularity and an increase in g-ratio of myelinated fibers and a decrease of unmyelinated fibers in the sural nerves of the gcg−/− mice. Effects of glucagon on neurite outgrowth were examined using an ex vivo culture of dorsal root ganglia. A supraphysiological concentration of glucagon promoted neurite outgrowth. In conclusion, the mice with deficiency of GCGDPs developed peripheral neuropathy with age. Furthermore, glucagon might have neuroprotective effects on the PNS of mice. GCGDPs might be involved in the pathology of DPN. |
| Databáze: | OpenAIRE |
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