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Selectively Bred Diabetes Models : GK Rats, NSY Mice, and ON Mice

Nagao, Mototsugu LU ; Esguerra, Jonathan Lou S LU orcid ; Wendt, Anna LU ; Asai, Akira LU ; Sugihara, Hitoshi ; Oikawa, Shinichi and Eliasson, Lena LU orcid (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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Please use this url to cite or link to this publication:
author
; ; ; ; ; and
organization
publishing date
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
978-1-0716-0384-0
978-1-0716-0385-7
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
2024-06-13 13:18:46
@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         = {{978-1-0716-0384-0}},
  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}},
}