Selectively Bred Diabetes Models : GK Rats, NSY Mice, and ON Mice
(2020) In Methods in molecular biology (Clifton, N.J.) 2128. p.25-54- Abstract
The polygenic background of selectively bred diabetes models mimics the etiology of type 2 diabetes. So far, three different rodent models (Goto-Kakizaki rats, Nagoya-Shibata-Yasuda mice, and Oikawa-Nagao mice) have been established in the diabetes research field by continuous selective breeding for glucose tolerance from outbred rodent stocks. The origin of hyperglycemia in these rodents is mainly insulin secretion deficiency from the pancreatic β-cells and mild insulin resistance in insulin target organs. In this chapter, we summarize backgrounds and phenotypes of these rodent models to highlight their importance in diabetes research. Then, we introduce experimental methodologies to evaluate β-cell exocytosis as a putative common... (More)
The polygenic background of selectively bred diabetes models mimics the etiology of type 2 diabetes. So far, three different rodent models (Goto-Kakizaki rats, Nagoya-Shibata-Yasuda mice, and Oikawa-Nagao mice) have been established in the diabetes research field by continuous selective breeding for glucose tolerance from outbred rodent stocks. The origin of hyperglycemia in these rodents is mainly insulin secretion deficiency from the pancreatic β-cells and mild insulin resistance in insulin target organs. In this chapter, we summarize backgrounds and phenotypes of these rodent models to highlight their importance in diabetes research. Then, we introduce experimental methodologies to evaluate β-cell exocytosis as a putative common defect observed in these rodent models.
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- author
- Nagao, Mototsugu LU ; Esguerra, Jonathan Lou S LU ; Wendt, Anna LU ; Asai, Akira LU ; Sugihara, Hitoshi ; Oikawa, Shinichi and Eliasson, Lena LU
- organization
- publishing date
- 2020-03-17
- type
- Chapter in Book/Report/Conference proceeding
- publication status
- published
- subject
- host publication
- Animal Models of Diabetes. Methods in Molecular Biology
- series title
- Methods in molecular biology (Clifton, N.J.)
- editor
- King, A
- volume
- 2128
- pages
- 30 pages
- publisher
- Humana Press
- external identifiers
-
- pmid:32180184
- scopus:85082023780
- ISSN
- 1940-6029
- ISBN
- 978-1-0716-0385-7
- 978-1-0716-0384-0
- DOI
- 10.1007/978-1-0716-0385-7_3
- language
- English
- LU publication?
- yes
- id
- 98cdca15-9e6a-4ecb-802b-23029a5af5c4
- date added to LUP
- 2020-03-22 14:52:40
- date last changed
- 2024-09-04 18:46:07
@inbook{98cdca15-9e6a-4ecb-802b-23029a5af5c4, abstract = {{<p>The polygenic background of selectively bred diabetes models mimics the etiology of type 2 diabetes. So far, three different rodent models (Goto-Kakizaki rats, Nagoya-Shibata-Yasuda mice, and Oikawa-Nagao mice) have been established in the diabetes research field by continuous selective breeding for glucose tolerance from outbred rodent stocks. The origin of hyperglycemia in these rodents is mainly insulin secretion deficiency from the pancreatic β-cells and mild insulin resistance in insulin target organs. In this chapter, we summarize backgrounds and phenotypes of these rodent models to highlight their importance in diabetes research. Then, we introduce experimental methodologies to evaluate β-cell exocytosis as a putative common defect observed in these rodent models.</p>}}, author = {{Nagao, Mototsugu and Esguerra, Jonathan Lou S and Wendt, Anna and Asai, Akira and Sugihara, Hitoshi and Oikawa, Shinichi and Eliasson, Lena}}, booktitle = {{Animal Models of Diabetes. Methods in Molecular Biology}}, editor = {{King, A}}, isbn = {{978-1-0716-0385-7}}, issn = {{1940-6029}}, language = {{eng}}, month = {{03}}, pages = {{25--54}}, publisher = {{Humana Press}}, series = {{Methods in molecular biology (Clifton, N.J.)}}, title = {{Selectively Bred Diabetes Models : GK Rats, NSY Mice, and ON Mice}}, url = {{http://dx.doi.org/10.1007/978-1-0716-0385-7_3}}, doi = {{10.1007/978-1-0716-0385-7_3}}, volume = {{2128}}, year = {{2020}}, }