Igel M, Becker W, Herberg L, Joost H G
Institut für Pharmakologie und Toxikologie der RWTH Aachen, Germany.
Horm Metab Res. 1996 Dec;28(12):669-73. doi: 10.1055/s-2007-979875.
NON mice exhibit a polygenic syndrome of mild obesity which is less pronounced than that of the ob and db strains. Here, we have shown that the syndrome is accompanied by a rise in leptin mRNA levels in adipose tissue, corresponding with the increase in adipose tissue mass. Surprisingly, levels of the leptin protein in adipose tissue and serum were comparable to those of lean control animals (BL57/Ksj-+/+), and markedly lower than those in db/db-mice. The coding regions of the cDNA sequences of both leptin and the leptin receptor from NON mice were identical with those of the wild-type sequences. We suggested that low levels of leptin in adipose tissue and serum contribute to the obesity of NON mice.
NON小鼠表现出一种轻度肥胖的多基因综合征，其症状不如ob和db品系明显。在此，我们发现该综合征伴随着脂肪组织中瘦素mRNA水平的升高，这与脂肪组织质量的增加相对应。令人惊讶的是，脂肪组织和血清中瘦素蛋白的水平与瘦对照动物（BL57/Ksj-+/+）相当，且明显低于db/db小鼠。NON小鼠的瘦素及其受体的cDNA序列编码区与野生型序列相同。我们认为，脂肪组织和血清中低水平的瘦素导致了NON小鼠的肥胖。
