Reichart U, Renner-Müller I, Höflich A, Müller O J, Franz W M, Wolf E, Müller M, Brem G, Aigner B
Institut für Tierzucht und Genetik, Veterinärmedizinische Universität Wien, Veterinärplatz 1, Vienna, A-1210, Austria.
Biochem Biophys Res Commun. 2000 Mar 16;269(2):502-7. doi: 10.1006/bbrc.2000.2318.
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.
非胰岛素依赖型糖尿病（2型糖尿病）是一种多基因和多因素疾病。在此，我们描述了一个转基因小鼠品系的长期研究，该品系显示由于转基因插入导致瘦素受体（Lepr，Ob-R）基因的破坏。长亚型Ob-Rb表达的缺失揭示了所使用的远交系纯合突变小鼠中肥胖和糖尿病表型的强烈差异。一部分纯合小鼠出现严重的持续性早发性肥胖，而另一部分在产后26周的检查期内出现初始肥胖后发展为恶病质。该品系的瘦素受体缺陷小鼠可能作为一种模型，用于研究调节糖尿病发生发展和表达模式的基因。
