以表彰他們的研究工作導致發現瘦素：一種調節食物攝入量和體重的激素。
人類肥瘦不一，原因是每個人控制體重的能力各異。肥胖通常與胰島素耐受和糖尿病相關聯，而這兩種疾病在很多國家的人口中，發病率頗高，幾乎算得上是疫症。道格拉斯·高爾曼( Douglas L Coleman)從事這方面的研究，取得重要成果，引導傑弗理·弗理德曼(Jeffrey M Friedman)的進一步工作，發現了相關的激素，從而使我們對調節體重的生物學途徑有了更深入的了解。
高爾曼在美國緬因州Bar Harbor傑克遜實驗室工作，率先開展了這方面的研究。高爾曼研究了兩品系的老鼠(ob/ob和db/db)，牠們都有嚴重病態肥胖和糖尿病。疾病分別是由兩種不同的純合隱性突變造成的。高爾曼懷疑ob/ob老鼠缺乏一種循環激素，引致肥胖，而db/db老鼠則過量製造這種激素，因而肥胖。於是他採用聯體技術(parabiosis)，把兩種老鼠的血管連接起來，發現ob/ob老鼠停止進食，體重降低，而db/db老鼠還是肥胖。高爾曼認為ob/ob老鼠不能製造一種抑制食慾的激素，而db/db老鼠則過量製造了這種激素，卻缺乏該激素的受體，所以不能傳遞激素的信息。當兩種老鼠的循環系統連接以後，抗肥胖激素從db/db老鼠進入ob/ob老鼠的體內，使之體重降低。而db/db老鼠由於缺乏相應的受體，體重沒有變化。
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.
