Clark J B, Palmer C J, Shaw W N
Proc Soc Exp Biol Med. 1983 May;173(1):68-75. doi: 10.3181/00379727-173-41611.
A noninsulin-dependent diabetes appeared in fatty rats in our Zucker rat colony. A breeding program yielded a genetic pattern of diabetes consistent with a dominant gene not closely linked to the fatty gene. Fatty males were more frequently affected than fatty females. Since no markers could be identified for heterozygous carriers and since affected fatty rats were 6 months old when diabetes appeared, the diabetic trait could not be sustained in our small colony. Glucose tolerance tests showed that the diabetic fatty rats had little increase in plasma insulin concentration after a glucose load was administered. Plasma insulin concentrations were unchanged relative to control fatty rats. Percentage body fat and plasma triglyceride values were decreased in fatty diabetic rats relative to control fatty rats, however, consistent with insulin resistance in fat and liver. The content of pancreatic insulin was markedly decreased in the diabetic fatty rat relative to either the ad libitum or diet-restricted fatty rats. The occurrence of a genetically based diabetes in a normally outbred colony underscores the importance of genetic traits that interact with obesity in determining diabetes in rodent models.
在我们的Zucker大鼠群体中，肥胖大鼠出现了非胰岛素依赖型糖尿病。一项育种计划产生了一种糖尿病的遗传模式，该模式与一个不与肥胖基因紧密连锁的显性基因一致。肥胖雄性大鼠比肥胖雌性大鼠更易受影响。由于无法识别杂合子携带者的标记，且受影响的肥胖大鼠在出现糖尿病时已6个月大，因此这种糖尿病性状在我们的小群体中无法持续。葡萄糖耐量试验表明，给予葡萄糖负荷后，糖尿病肥胖大鼠的血浆胰岛素浓度几乎没有增加。相对于对照肥胖大鼠，血浆胰岛素浓度没有变化。然而，与对照肥胖大鼠相比，糖尿病肥胖大鼠的体脂百分比和血浆甘油三酯值降低，这与脂肪和肝脏中的胰岛素抵抗一致。相对于自由采食或限食的肥胖大鼠，糖尿病肥胖大鼠胰腺胰岛素含量明显降低。在一个正常远交群体中出现基于遗传的糖尿病，凸显了在啮齿动物模型中，与肥胖相互作用的遗传性状在决定糖尿病方面的重要性。
