Name: Crl:ZUC- Lepr fa
Creator: Rat Genome Database
License: Creative Commons CC BY 4.0
Keywords: Rat Gene RGD Genome

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Strain: Crl:ZUC-Lepr^fa
Symbol:	Crl:ZUC-Lepr^fa
Strain:	ZUC-Lepr^fa
Substrain:	Crl
Full Name:	Zucker rats
RGD ID:	1357184
Citation ID:	RRID:RGD_1357184
Ontology ID:	RS:0001837
Alleles:	Lepr^fa
Variant(s):	Leprfa-var1
Also Known As:	ZUC-Lepr^fa; Crl:ZUC-Lepr^fa; Crl:(ZUC)faBR; Crl:ZUC-Leprfa; Crl:ZUC-Lepr^[fa]
Type:	outbred
Available Source:	Charles River Laboratories
Origination:	Charles River Laboratories
Description:	The obese and fatty condition appeared spontaneously in the 13M stock and was reported by Lois Zucker and Theodore Zucker in 1960 at the Laboratory of Comparative Pathology in Stow, Massachusetts. These came to Charles River in 1985 from a research colony maintained at a pharmaceutical company.
Last Known Status:	Unknown

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References

References - curated

#	Reference Title	Reference Citation
1.	Modulation of adipoinsular axis in prediabetic zucker diabetic fatty rats by diazoxide.	Alemzadeh R and Tushaus KM, Endocrinology 2004 Dec;145(12):5476-84. Epub 2004 Aug 19.
2.	Diazoxide enhances adipose tissue protein kinase B activation and glucose transporter-4 expression in obese Zucker rats.	Alemzadeh R, etal., Med Sci Monit 2004 Mar;10(3):BR53-60. Epub 2004 Mar 1.
3.	Preferential channeling of energy fuels toward fat rather than muscle during high free fatty acid availability in rats.	Fabris R, etal., Diabetes 2001 Mar;50(3):601-8.
4.	Strains registered by Charles River Laboratories International, Inc.	Personal communication with Charles River Laboratories
5.	RGD Strain RSO annotation pipeline	RGD Automated Pipelines

Region

Allelic Variants

Additional Information

RGD Curation Notes

Note Type	Note	Reference
strain_drgs_chems	Diazoxide (an inhibitor of insulin secretion) helped in reducing the food intake and the rate of weight gain; this also helped in preventing beta-cell failure and progression of diabetes.	1354693
strain_drgs_chems	Adipose tissues from the animals treated with diazoxide showed enhanced protein kinase B/Akt and Glut-4 expression that resulted in increased glucose uptake.	1354694
strain_life_disease	These are a good model for type 2 diabetes and they have chronic hyperinsulinemia,	1354693
strain_phys_biochem	High nonesterified fatty acid (NEFA) levels markedly deceased insulin-mediated glucose uptake in red fiber-type muscles but enhanced glucose utilization in visceral fat. NEFA are involved in the partioning calories to fat by modulating in vivo gene expression of FTA/CD36, Glut4, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 in visceral and red fiber-type muscle.	68925

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