Contrasting obesity phenotypes uncovered by partial leptin receptor gene deletion in transgenic mice.
Biochem Biophys Res Commun
; 269(2): 502-7, 2000 Mar 16.
Article
in En
| MEDLINE
| ID: mdl-10708583
ABSTRACT
Non-insulin-dependent diabetes mellitus (type 2 diabetes) is known to be a polygenic and polyfactorial disorder. Here we describe the long-term examination of a transgenic mouse line showing the disruption of the leptin receptor (Lepr, Ob-R) gene caused by transgene insertion. The absence of the expression of the long isoform Ob-Rb uncovered a strong variation of the obesity and diabetes phenotype in the homozygous mutant mice of the outbred strain used. One part of the homozygous mice developed severe persistent early-onset obesity, whereas the other part developed cachexia after having shown initial obesity in the examination period up to 26 weeks p.p. The leptin-receptor-defective mice of this line might serve as a model for the investigation of genes modulating the development and mode of expression of diabetes.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Carrier Proteins
/
Gene Deletion
/
Receptors, Cell Surface
/
Obesity
Limits:
Animals
Language:
En
Journal:
Biochem Biophys Res Commun
Year:
2000
Document type:
Article