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Experimental Physiology 93.2 pp 213-222
DOI: 10.1113/expphysiol.2007.039222
© The Physiological Society 2008
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Sensory and autonomic nerve changes in the monosodium glutamate-treated rat: a model of type II diabetes

John F. B. Morrison1, Safa Shehab2, Rajan Sheen3, Subramanian Dhanasekaran1, Mohammed Shaffiullah3 and Eric Mensah-Brown2

Departments of 1 Physiology2 Anatomy3 Pharmacology, Faculty of Medicine and Health Sciences, United Arab Emirates University, PO Box 17666, Al Ain, United Arab Emirates

Rats that had been injected with monosodium glutamate (MSG) neonatally were studied for up to 70 weeks and compared with age-matched control rats to study changes in glucose tolerance and in sympathetic and sensory nerves. At 61 and 65 weeks of age, there were significant differences in glucose tolerance between the MSG and control groups, and the MSG group had raised fasting blood glucose. These changes were not associated with changes in the number of β-cells in the islets of Langerhans. In addition, the diabetic MSG-treated rats had central obesity and cataracts. Hypoalgesia to thermal stimuli was present in MSG-treated rats as early as 6 weeks and persisted at 70 weeks. However, no differences were observed in the distribution of substance P, the neurokinin-1 receptor or calcitonin gene-related peptide in the dorsal horn of L3–L5 at this age (70 weeks). Diabetic MSG-treated animals at 65 and 70 weeks of age had significantly reduced noradrenaline concentrations in the heart, tail artery and ileum, while concentrations in the adrenal gland and corpus cavernosum were significantly increased. There was also a significant increase in adrenal adrenaline, dopamine and serotonin, largely attributable to changes in weight of the adrenal gland in the MSG-treated animals. The results indicate that MSG-treated animals develop a form of type II diabetes by about 60 weeks of age, and that there are significant changes in amine levels in various tissues associated with these developments.

(Received 25 June 2007; accepted after revision 1 October 2007; first published online 2 October 2007)
Corresponding author J. F. B. Morrison: Department of Physiology, Faculty of Medicine and Health Sciences, United Arab Emirates University, PO Box 17666, Al Ain, United Arab Emirates. Email: john.morrison{at}uaeu.ac.ae







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