以表彰他们的研究工作导致发现瘦素：一种调节食物摄入量和体重的激素。
人类肥瘦不一，原因是每个人控制体重的能力各异。肥胖通常与胰岛素耐受和糖尿病相关联，而这两种疾病在很多国家的人口中，发病率颇高，几乎算得上是疫症。道格拉斯·高尔曼( Douglas L Coleman)从事这方面的研究，取得重要成果，引导杰弗理·弗理德曼(Jeffrey M Friedman)的进一步工作，发现了相关的激素，从而使我们对调节体重的生物学途径有了更深入的了解。
高尔曼在美国缅因州Bar Harbor杰克逊实验室工作，率先开展了这方面的研究。高尔曼研究了两品系的老鼠(ob/ob和db/db)，它们都有严重病态肥胖和糖尿病。疾病分别是由两种不同的纯合隐性突变造成的。高尔曼怀疑ob/ob老鼠缺乏一种循环激素，引致肥胖，而db/db老鼠则过量制造这种激素，因而肥胖。於是他采用联体技术(parabiosis)，把两种老鼠的血管连接起来，发现ob/ob老鼠停止进食，体重降低，而db/db老鼠还是肥胖。高尔曼认为ob/ob老鼠不能制造一种抑制食欲的激素，而db/db老鼠则过量制造了这种激素，却缺乏该激素的受体，所以不能传递激素的信息。当两种老鼠的循环系统连接以后，抗肥胖激素从db/db老鼠进入ob/ob老鼠的体内，使之体重降低。而db/db老鼠由於缺乏相应的受体，体重没有变化。
Individuals vary in their ability to control body weight. Obesity is frequently associated with insulin resistance and diabetes, which often leads to heart, kidney and other diseases. Obesity is an important health problem and has reached epidemic proportions in many countries. The discovery by Douglas L Coleman led the way to the work of Jeffrey M Friedman, who uncovered a hormone that increased our understanding of the biological pathways that regulate body weight.
These studies began with the work of Douglas L Coleman at The Jackson Laboratories in Bar Harbor, Maine, USA. Coleman investigated two strains of mice (ob/ob and db/db), both of which exhibit grossly morbid obesity and severe diabetes caused by homozygosity, for two different recessive mutations. Coleman suspected that the ob/ob mice lacked a circulating hormone whereas the db/db mice overproduced it. So, he performed experiments in which the circulations of these 2 different strains of mice were joined together in a technique called parabiosis. When attached to a db/db mouse, the ob/ob mouse stopped eating and lost weight, while the db/db mouse remained obese. Coleman concluded that the ob/ob mice failed to produce a functional hormone that inhibits eating whereas the db/db mice overproduced the hormone, but lacked the receptor necessary to receive and transmit the hormone signal. When the circulations of ob/ob and db/db mice were joined during the parabiosis, the anti-obesity hormone from the db/db mouse crossed into the ob/ob mouse and induced its weight loss. The db/db mouse showed no change in body weight because it lacked the receptor for this hormone and therefore remained obese.
