Bchini O, Mehtali M, Lathe R
LGME-CNRS and U184-INSERM, Strasbourg, France.
J Mol Endocrinol. 1991 Apr;6(2):129-35. doi: 10.1677/jme.0.0060129.
Glucose tolerance was studied in transgenic mice (SJL x C57BL/6) expressing human GH under the control of a housekeeping promoter. Parental SJL mice were found to harbour a dominant allele, termed here glid, determining glucose intolerance in pure-bred animals and in F1 hybrids with glucose-tolerant C57BL/6 mice. Blood glucose levels in transgenic SJL x C57BL/6 hybrid mice were well controlled following glucose challenge, whereas non-transgenic hybrids failed to control their glucose adequately. Pancreatic morphology was normal in all animals. In confirmation of a physiological role for GH in glucose regulation. GH-deficient lit/lit mice were pathologically sensitive to glucose.
在由管家启动子控制下表达人生长激素（GH）的转基因小鼠（SJL×C57BL/6）中研究了葡萄糖耐量。发现亲代SJL小鼠携带一个显性等位基因，在此称为glid，该基因决定了纯种动物以及与糖耐量正常的C57BL/6小鼠的F1杂种中的葡萄糖不耐受性。葡萄糖激发后，转基因SJL×C57BL/6杂种小鼠的血糖水平得到良好控制，而非转基因杂种小鼠则无法充分控制其血糖。所有动物的胰腺形态均正常。为证实生长激素在葡萄糖调节中的生理作用，生长激素缺乏的lit/lit小鼠对葡萄糖具有病理敏感性。
