Contrasting obesity phenotypes uncovered by partial leptin receptor gene deletion in transgenic mice.
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.
Reichart
U
U
Institut für Tierzucht und Genetik, Veterinärmedizinische Universität Wien, Veterinärplatz 1, Vienna, A-1210, Austria.
Renner-Müller
I
I
Höflich
A
A
Müller
O J
OJ
Franz
W M
WM
Wolf
E
E
Müller
M
M
Brem
G
G
Aigner
B
B
D000818:Animals; D001835:Body Weight / Q000235:genetics; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics; D005260:Female; D017353:Gene Deletion; D006720:Homozygote; D020738:Leptin / Q000097:blood; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D008822:Mice, Transgenic; D009765:Obesity / Q000235:genetics*; D010641:Phenotype; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin
D002352:Carrier Proteins; D020738:Leptin; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; C515447:leptin receptor, mouse