Coleman D L
Int J Obes. 1985;9 Suppl 2:69-73.
Several different single gene mutations are known to cause similar diabetes-obesity syndromes in mice. Our studies with two mutations, obese (ob) and diabetes (db) have shown that each syndrome develops similarly. Symptoms include hyperinsulinemia, hyperglycemia, hyperphagia, diabetes, and obesity coupled with similar, and large increases, in the efficiency of food utilization. Even when maintained on 50 percent of normal food intake, mutants still become obese. This increase in metabolic efficiency has been suggested to be due to a failure of mutant mice to thermoregulate. Our studies indicate that any defect in thermoregulation is not severe enough to conserve sufficient calories to account for the large increase in metabolic efficiency observed in each mutant and the increased efficiency seen in mutants must be a result of other mechanisms. More critical studies in both normal and obese mice should lead to information defining the contribution of the many different potential energy saving mechanisms available.
已知几种不同的单基因突变会在小鼠中引发类似的糖尿病 - 肥胖综合征。我们对肥胖（ob）和糖尿病（db）这两种突变的研究表明，每种综合征的发展过程相似。症状包括高胰岛素血症、高血糖、食欲亢进、糖尿病和肥胖，同时食物利用效率也有相似且大幅的提高。即使将食物摄入量维持在正常水平的50%，突变小鼠仍会肥胖。有人认为这种代谢效率的提高是由于突变小鼠体温调节功能失效。我们的研究表明，任何体温调节缺陷都不够严重，无法节省足够的热量来解释在每个突变体中观察到的代谢效率大幅提高，而且突变体中观察到的效率提高必定是其他机制导致的。对正常小鼠和肥胖小鼠进行更深入的研究应该能得出明确多种不同潜在节能机制作用的信息。
