Coleman D L
Science. 1979 Feb 16;203(4381):663-5. doi: 10.1126/science.760211.
The mouse mutant genes obese (ob) and diabetes (db) cause similar obesity-diabetes states in homozygotes. These obesity syndromes are characterized by a more efficient conversion of food to lipid and, once stored, a slower rate of catabolism on fasting. Heterozygous mice, either ob/+ or db/+, survived a prolonged fast significantly longer than normal homozygotes (+/+); this suggests that the heterozygotes exhibited increased metabolic efficiency, a feature normally associated with both homozygous mutants. The existence of this thriftiness trait, if manifested by heterozygous carriers in wild populations, would lend credence to the thrifty gene concept of diabetes. Beneficial effects of normally deleterious genes may have played a role in the development of diabetes-susceptible human populations, as well as having provided the survival advantage that has allowed both the development and successful establishment of species in desert and other less affluent regions.
小鼠突变基因肥胖（ob）和糖尿病（db）在纯合子中会导致相似的肥胖 - 糖尿病状态。这些肥胖综合征的特征是食物向脂质的转化效率更高，且一旦储存，禁食时的分解代谢速率较慢。杂合子小鼠，即ob/+ 或db/+，在长时间禁食后的存活时间明显长于正常纯合子（+/+）；这表明杂合子表现出更高的代谢效率，这是通常与两种纯合突变体相关的特征。如果野生种群中的杂合子携带者表现出这种节俭性状，将为糖尿病的节俭基因概念提供支持。正常情况下有害的基因所产生的有益影响，可能在糖尿病易感人群的发展中发挥了作用，同时也提供了生存优势，使得物种能够在沙漠和其他资源较匮乏的地区得以发展并成功生存。
