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Biochem Biophys Res Commun. 2000 Mar 16;269(2):502-7.

Contrasting obesity phenotypes uncovered by partial leptin receptor gene deletion in transgenic mice.

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1
Institut für Tierzucht und Genetik, Veterinärmedizinische Universität Wien, Veterinärplatz 1, Vienna, A-1210, Austria.

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.

PMID:
10708583
DOI:
10.1006/bbrc.2000.2318
[Indexed for MEDLINE]
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