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Preliminary Characterization of a Leptin Receptor Knockout Rat Created by CRISPR/Cas9 System.

Authors: Bao, Dan  Ma, Yuanwu  Zhang, Xu  Guan, Feifei  Chen, Wei  Gao, Kai  Qin, Chuan  Zhang, Lianfeng 
Citation: Bao D, etal., Sci Rep. 2015 Nov 5;5:15942. doi: 10.1038/srep15942.
Pubmed: (View Article at PubMed) PMID:26537785
DOI: Full-text: DOI:10.1038/srep15942

Leptin receptor, which is encoded by the diabetes (db) gene and is highly expressed in the choroid plexus, regulatesenergy homeostasis, the balance between food intake and energy expenditure, fertility and bone mass. Here, using CRISPR/Cas9 technology, we created the leptin receptor knockout rat. Homozygous leptin receptor null rats are characterized by obesity, hyperphagia, hyperglycemia, glucose intolerance, hyperinsulinemia and dyslipidemia. Due to long-term poor glycemic control, the leptin receptor knockout rats also develop some diabetic complications such as pancreatic, hepatic and renal lesions. In addition, the leptin receptor knockout rats show a significant decrease in bone volume and bone mineral density of the femur compared with their wild-type littermates. Our model has rescued some deficiency of the existing rodent models, such as the transient hyperglycemia of db/db mice in the C57BL/6J genetic background and the delayed onset of glucose intolerance in the Zucker rats, and it is proven to be a useful animal model for biomedical and pharmacological research on obesity and diabetes.


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CRRD Object Information
CRRD ID: 12911216
Created: 2017-07-07
Species: All species
Last Modified: 2017-07-07
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.