Sensory and autonomic nerve changes in the monosodium glutamate-treated rat: a model of type II diabetes
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 tole...
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| Veröffentlicht in: | Experimental physiology 2008-02, Vol.93 (2), p.213-222 |
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| creator | Morrison, John F. B. Shehab, Safa Sheen, Rajan Dhanasekaran, Subramanian Shaffiullah, Mohammed Mensah‐Brown, Eric |
| description | 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 L3âL5 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. |
| doi_str_mv | 10.1113/expphysiol.2007.039222 |
| format | Article |
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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 L3âL5 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.</description><identifier>ISSN: 0958-0670</identifier><identifier>EISSN: 1469-445X</identifier><identifier>DOI: 10.1113/expphysiol.2007.039222</identifier><identifier>PMID: 17911358</identifier><language>eng</language><publisher>Oxford, UK: The Physiological Society</publisher><subject>Aging - physiology ; Animals ; Autonomic Nervous System - physiology ; Blood Glucose - metabolism ; Body Weight - physiology ; Calcitonin Gene-Related Peptide - metabolism ; Chromatography, High Pressure Liquid ; Diabetes Mellitus, Type 2 - chemically induced ; Diabetes Mellitus, Type 2 - pathology ; Diabetes Mellitus, Type 2 - physiopathology ; Diabetic Neuropathies - pathology ; Diabetic Neuropathies - physiopathology ; Glucose Intolerance - chemically induced ; Glucose Intolerance - physiopathology ; Glucose Tolerance Test ; Hot Temperature ; Immunohistochemistry ; Insulin - metabolism ; Insulin-Secreting Cells - drug effects ; Insulin-Secreting Cells - metabolism ; Neurons, Afferent - physiology ; Obesity - complications ; Organ Size - physiology ; Pain Measurement - drug effects ; Physical Stimulation ; Radioimmunoassay ; Rats ; Rats, Wistar ; Receptors, Neurokinin-1 - metabolism ; Sodium Glutamate ; Substance P - metabolism</subject><ispartof>Experimental physiology, 2008-02, Vol.93 (2), p.213-222</ispartof><rights>Journal compilation © 2008 The Physiological Society</rights><rights>2007 The Authors. Journal compilation © 2007 The Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4992-45219a1056ec76e1f2b7471ca81bfe7eae3fa99acfb19900caeed8386bf6d48e3</citedby><cites>FETCH-LOGICAL-c4992-45219a1056ec76e1f2b7471ca81bfe7eae3fa99acfb19900caeed8386bf6d48e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1113%2Fexpphysiol.2007.039222$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1113%2Fexpphysiol.2007.039222$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17911358$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morrison, John F. B.</creatorcontrib><creatorcontrib>Shehab, Safa</creatorcontrib><creatorcontrib>Sheen, Rajan</creatorcontrib><creatorcontrib>Dhanasekaran, Subramanian</creatorcontrib><creatorcontrib>Shaffiullah, Mohammed</creatorcontrib><creatorcontrib>Mensah‐Brown, Eric</creatorcontrib><title>Sensory and autonomic nerve changes in the monosodium glutamate-treated rat: a model of type II diabetes</title><title>Experimental physiology</title><addtitle>Exp Physiol</addtitle><description>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 L3âL5 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.</description><subject>Aging - physiology</subject><subject>Animals</subject><subject>Autonomic Nervous System - physiology</subject><subject>Blood Glucose - metabolism</subject><subject>Body Weight - physiology</subject><subject>Calcitonin Gene-Related Peptide - metabolism</subject><subject>Chromatography, High Pressure Liquid</subject><subject>Diabetes Mellitus, Type 2 - chemically induced</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Diabetes Mellitus, Type 2 - physiopathology</subject><subject>Diabetic Neuropathies - pathology</subject><subject>Diabetic Neuropathies - physiopathology</subject><subject>Glucose Intolerance - chemically induced</subject><subject>Glucose Intolerance - physiopathology</subject><subject>Glucose Tolerance Test</subject><subject>Hot Temperature</subject><subject>Immunohistochemistry</subject><subject>Insulin - metabolism</subject><subject>Insulin-Secreting Cells - drug effects</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>Neurons, Afferent - physiology</subject><subject>Obesity - complications</subject><subject>Organ Size - physiology</subject><subject>Pain Measurement - drug effects</subject><subject>Physical Stimulation</subject><subject>Radioimmunoassay</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Neurokinin-1 - metabolism</subject><subject>Sodium Glutamate</subject><subject>Substance P - metabolism</subject><issn>0958-0670</issn><issn>1469-445X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU2L1TAYhYMoznX0LwzBhbjpNV9tk9nJMDoXBhRUcBfS9O1thrapSerYf28uvTDgytW7yHMewjkIXVGyp5TyD_Bnnvs1Oj_sGSH1nnDFGHuGdlRUqhCi_Pkc7YgqZUGqmlygVzE-EEI5keIluqC1ypJS7lD_Dabow4rN1GKzJD_50Vk8QfgN2PZmOkLEbsKpBzzmx-hbt4z4OCzJjCZBkQLk0-Jg0jU2mWlhwL7DaZ0BHw64daaBBPE1etGZIcKb871EPz7dfr-5K-6_fD7cfLwvrFCKFaJkVBlKygpsXQHtWFOLmlojadNBDQZ4Z5QytmuoUoRYA9BKLqumq1ohgV-i95t3Dv7XAjHp0UULw2Am8EvUVCoq69xDldG3_6APfglT_p1muc-ac3qCqg2ywccYoNNzcKMJq6ZEn6bQT1Po0xR6myIHr872pRmhfYqdu8_A9QY8ugHW_9Tq2693Qpzs77Zw7479owugNzh66yCtWnHNNKOc_wXowKmG</recordid><startdate>200802</startdate><enddate>200802</enddate><creator>Morrison, John F. B.</creator><creator>Shehab, Safa</creator><creator>Sheen, Rajan</creator><creator>Dhanasekaran, Subramanian</creator><creator>Shaffiullah, Mohammed</creator><creator>Mensah‐Brown, Eric</creator><general>The Physiological Society</general><general>Blackwell Publishing Ltd</general><general>John Wiley & Sons, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7TS</scope></search><sort><creationdate>200802</creationdate><title>Sensory and autonomic nerve changes in the monosodium glutamate-treated rat: a model of type II diabetes</title><author>Morrison, John F. B. ; Shehab, Safa ; Sheen, Rajan ; Dhanasekaran, Subramanian ; Shaffiullah, Mohammed ; Mensah‐Brown, Eric</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4992-45219a1056ec76e1f2b7471ca81bfe7eae3fa99acfb19900caeed8386bf6d48e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Aging - physiology</topic><topic>Animals</topic><topic>Autonomic Nervous System - physiology</topic><topic>Blood Glucose - metabolism</topic><topic>Body Weight - physiology</topic><topic>Calcitonin Gene-Related Peptide - metabolism</topic><topic>Chromatography, High Pressure Liquid</topic><topic>Diabetes Mellitus, Type 2 - chemically induced</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Diabetes Mellitus, Type 2 - physiopathology</topic><topic>Diabetic Neuropathies - pathology</topic><topic>Diabetic Neuropathies - physiopathology</topic><topic>Glucose Intolerance - chemically induced</topic><topic>Glucose Intolerance - physiopathology</topic><topic>Glucose Tolerance Test</topic><topic>Hot Temperature</topic><topic>Immunohistochemistry</topic><topic>Insulin - metabolism</topic><topic>Insulin-Secreting Cells - drug effects</topic><topic>Insulin-Secreting Cells - metabolism</topic><topic>Neurons, Afferent - physiology</topic><topic>Obesity - complications</topic><topic>Organ Size - physiology</topic><topic>Pain Measurement - drug effects</topic><topic>Physical Stimulation</topic><topic>Radioimmunoassay</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Neurokinin-1 - metabolism</topic><topic>Sodium Glutamate</topic><topic>Substance P - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morrison, John F. B.</creatorcontrib><creatorcontrib>Shehab, Safa</creatorcontrib><creatorcontrib>Sheen, Rajan</creatorcontrib><creatorcontrib>Dhanasekaran, Subramanian</creatorcontrib><creatorcontrib>Shaffiullah, Mohammed</creatorcontrib><creatorcontrib>Mensah‐Brown, Eric</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><jtitle>Experimental physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morrison, John F. B.</au><au>Shehab, Safa</au><au>Sheen, Rajan</au><au>Dhanasekaran, Subramanian</au><au>Shaffiullah, Mohammed</au><au>Mensah‐Brown, Eric</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sensory and autonomic nerve changes in the monosodium glutamate-treated rat: a model of type II diabetes</atitle><jtitle>Experimental physiology</jtitle><addtitle>Exp Physiol</addtitle><date>2008-02</date><risdate>2008</risdate><volume>93</volume><issue>2</issue><spage>213</spage><epage>222</epage><pages>213-222</pages><issn>0958-0670</issn><eissn>1469-445X</eissn><abstract>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 L3âL5 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.</abstract><cop>Oxford, UK</cop><pub>The Physiological Society</pub><pmid>17911358</pmid><doi>10.1113/expphysiol.2007.039222</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Experimental physiology, 2008-02, Vol.93 (2), p.213-222 |
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| source | Wiley Free Content; MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Aging - physiology Animals Autonomic Nervous System - physiology Blood Glucose - metabolism Body Weight - physiology Calcitonin Gene-Related Peptide - metabolism Chromatography, High Pressure Liquid Diabetes Mellitus, Type 2 - chemically induced Diabetes Mellitus, Type 2 - pathology Diabetes Mellitus, Type 2 - physiopathology Diabetic Neuropathies - pathology Diabetic Neuropathies - physiopathology Glucose Intolerance - chemically induced Glucose Intolerance - physiopathology Glucose Tolerance Test Hot Temperature Immunohistochemistry Insulin - metabolism Insulin-Secreting Cells - drug effects Insulin-Secreting Cells - metabolism Neurons, Afferent - physiology Obesity - complications Organ Size - physiology Pain Measurement - drug effects Physical Stimulation Radioimmunoassay Rats Rats, Wistar Receptors, Neurokinin-1 - metabolism Sodium Glutamate Substance P - metabolism |
| title | Sensory and autonomic nerve changes in the monosodium glutamate-treated rat: a model of type II diabetes |
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