Comparison of Two New Mouse Models of Polygenic Type 2 Diabetes at the Jackson Laboratory, NONcNZO10Lt/J and TALLYHO/JngJ
This review compares two novel polygenic mouse models of type 2 diabetes (T2D), TALLYHO/JngJ and NONcNZO10/LtJ, and contrasts both with the well-known C57BLKS/J-Leprdb (db/db) monogenic diabesity model. We posit that the new polygenic models are more representative of the “garden va...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Journal of Diabetes Research |
| Online Access: | http://dx.doi.org/10.1155/2013/165327 |
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| author | Edward H. Leiter Marjorie Strobel Adam O'Neill David Schultz Andrew Schile Peter C. Reifsnyder |
| author_facet | Edward H. Leiter Marjorie Strobel Adam O'Neill David Schultz Andrew Schile Peter C. Reifsnyder |
| author_sort | Edward H. Leiter |
| collection | DOAJ |
| description | This review compares two novel polygenic mouse models of type 2 diabetes (T2D), TALLYHO/JngJ and NONcNZO10/LtJ, and contrasts both with the well-known C57BLKS/J-Leprdb
(db/db) monogenic diabesity model. We posit that the new polygenic models are more representative of the “garden variety” obesity underlying human T2D in terms of their polygenetic rather than monogenic etiology. Moreover, the clinical phenotypes in these new models are less extreme, for example, more moderated development of obesity coupled with less extreme endocrine disturbances. The more progressive development of obesity produces a maturity-onset development of hyperglycemia in contrast to the juvenile-onset diabetes observed in the morbidly obese db/db model. Unlike the leptin receptor-deficient db/db models with central leptin resistance, the new models develop a progressive peripheral leptin resistance and are able to maintain reproductive function. Although the T2D pathophysiology in both TALLYHO/JngJ and NONcNZO10/LtJ is remarkably similar, their genetic etiologies are clearly different, underscoring the genetic heterogeneity underlying T2D in humans. |
| format | Article |
| id | doaj-art-3511f127ab5948e7bf699be37096a7b5 |
| institution | Kabale University |
| issn | 2314-6745 2314-6753 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Diabetes Research |
| spelling | doaj-art-3511f127ab5948e7bf699be37096a7b52025-02-03T01:30:32ZengWileyJournal of Diabetes Research2314-67452314-67532013-01-01201310.1155/2013/165327165327Comparison of Two New Mouse Models of Polygenic Type 2 Diabetes at the Jackson Laboratory, NONcNZO10Lt/J and TALLYHO/JngJEdward H. Leiter0Marjorie Strobel1Adam O'Neill2David Schultz3Andrew Schile4Peter C. Reifsnyder5The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USAThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USAThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USAThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USAThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USAThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USAThis review compares two novel polygenic mouse models of type 2 diabetes (T2D), TALLYHO/JngJ and NONcNZO10/LtJ, and contrasts both with the well-known C57BLKS/J-Leprdb (db/db) monogenic diabesity model. We posit that the new polygenic models are more representative of the “garden variety” obesity underlying human T2D in terms of their polygenetic rather than monogenic etiology. Moreover, the clinical phenotypes in these new models are less extreme, for example, more moderated development of obesity coupled with less extreme endocrine disturbances. The more progressive development of obesity produces a maturity-onset development of hyperglycemia in contrast to the juvenile-onset diabetes observed in the morbidly obese db/db model. Unlike the leptin receptor-deficient db/db models with central leptin resistance, the new models develop a progressive peripheral leptin resistance and are able to maintain reproductive function. Although the T2D pathophysiology in both TALLYHO/JngJ and NONcNZO10/LtJ is remarkably similar, their genetic etiologies are clearly different, underscoring the genetic heterogeneity underlying T2D in humans.http://dx.doi.org/10.1155/2013/165327 |
| spellingShingle | Edward H. Leiter Marjorie Strobel Adam O'Neill David Schultz Andrew Schile Peter C. Reifsnyder Comparison of Two New Mouse Models of Polygenic Type 2 Diabetes at the Jackson Laboratory, NONcNZO10Lt/J and TALLYHO/JngJ Journal of Diabetes Research |
| title | Comparison of Two New Mouse Models of Polygenic Type 2 Diabetes at the Jackson Laboratory, NONcNZO10Lt/J and TALLYHO/JngJ |
| title_full | Comparison of Two New Mouse Models of Polygenic Type 2 Diabetes at the Jackson Laboratory, NONcNZO10Lt/J and TALLYHO/JngJ |
| title_fullStr | Comparison of Two New Mouse Models of Polygenic Type 2 Diabetes at the Jackson Laboratory, NONcNZO10Lt/J and TALLYHO/JngJ |
| title_full_unstemmed | Comparison of Two New Mouse Models of Polygenic Type 2 Diabetes at the Jackson Laboratory, NONcNZO10Lt/J and TALLYHO/JngJ |
| title_short | Comparison of Two New Mouse Models of Polygenic Type 2 Diabetes at the Jackson Laboratory, NONcNZO10Lt/J and TALLYHO/JngJ |
| title_sort | comparison of two new mouse models of polygenic type 2 diabetes at the jackson laboratory noncnzo10lt j and tallyho jngj |
| url | http://dx.doi.org/10.1155/2013/165327 |
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