1997 Fiscal Year Final Research Report Summary
Dysfunction of the salivary gland in NOD mouse
| Project/Area Number |
07672199
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Tsurumi University |
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Principal Investigator |
NAKAGAWA Yoichi Tsurumi University, School of Dental Medicine, Lecturer, 歯学部, 講師 (90148057)
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| Project Period (FY) |
1995 – 1997
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| Keywords | Sjogren's syndrome / NOD mouse / salivary gland / signal transduction / neuropeptide / Insulin-like growth factor |
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| Research Abstract |
The non-obese diabetic (NOD) mouse has been recognized as an animal model for autoimmune type 1 insulin-dependent diabetes mellitus and has been shown a loss in secretory function of the salivary glands. To understand the salivary functional changes of the salivary gland in NOD mouse, the following investigations were carried out.
(1) The secretory response to muscarinic receptor stimulation : NOD showed a reduced potential for the generation of cAMP in the glands. Basal and agonist stimulated concentrations of inositol phosphate were reduced in submandibular gland of NOD mice. The receptor density was decreased in the glands. The reduction of muscarinic agonist response was suggested to be due to a generalized reduction in signal transduction components as a consequence of autoantibodies detected against cell surface antigens.
(2) The levels of neuropeptides and salivary gland responses : Injection of either of the three neuropeptides, substance P (SP), vasoactive intestinal polypeptide
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(VIP), and neuropeptide Y (NPY), in combination with the muscarinicchorinergic agonist pilocarpine increased saliva flow rates in Balb/c mice while threr was no observable augmentation to flow rates in NOD mice. Radioimmunoassay determination of neuropeptide concentrations in the submandibular and parotid glands revealed reduced levels of SP with diabetic onset. VIP concentrations were reduced in the submandibular gland of NOD mice. The findings suggested the dysfunction observed in NOD mice to be due to a general loss of neurotransmitter responsiveness on the part of salivary gland cells.
(3) Gastrointestinal absorption of Insulin-like growth factor (IGF) and the levels of Insulin-like growth factor binding protein (IGFBP) : IGFBP were detected in the sera, but not in the saliva. Gavage administration of radiolabeled IGF indicated substantial uptake from the gastrointestinal tract and significant tissue distribution. The tissue distribution in the diabetic NOD mouse was reduced, which suggest to contribute to reduced growth and wound healing potentials. Less
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[Publications] Yamamoto, H., Sims, E.S., Macauley, S.P., Nguyen, K-H.T., Nakagawa, Y.and Humphreys-Beher, M.G.: "Alteration in the secretory response of non-obese diabetic (NOD) mice to muscarinic receptor stimulation." Clinical Immunology and Immunopathology. 78(3). 245-255 (1996)
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「研究成果報告書概要(欧文)」より
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[Publications] Yamamoto, H., Ishibashi, K., Nakagawa, Y., Maeda, N., Zeng, T., Robinson, C.P., Oxford, g.E., Chegini, N.and Humphreys-Beher, M.G.: "Detection of alterations in the levels of neuropeptides and salivary gland responses in the non-obese diabetic mouse model for autoimmune sialoadenitis." Scand J Immunol. 45. 55-61 (1997)
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「研究成果報告書概要(欧文)」より
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[Publications] Nakagawa, Y., Oxford, G.E., Ishibasih, K., Yamamoto, H., Maeda, N., Bowen, E., Brayr, J., and Humphreys-Beher, M.G.: "Gastrointeistinal absorption of Insulin-like growth factor in the mouse in the absence of salivary insulin-like growth factor binding protein." Biochemical Pharmacology. 53. 233-240 (1997)
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「研究成果報告書概要(欧文)」より
