Douglas L. Coleman | |
|---|---|
| Born | Douglas Leonard Coleman[1] (1931-10-06)October 6, 1931 |
| Died | April 16, 2014(2014-04-16) (aged 82) |
| Education | McMaster University (BSc) University of Wisconsin–Madison (PhD) |
| Known for | Prediction of the existence ofleptin |
| Spouse | Beverly J. Benallick (died 2009) |
| Children | 3 |
| Awards | Canada Gairdner International Award Shaw Prize in Life science and Medicine Albert Lasker Award for Basic Medical Research BBVA Foundation Frontiers of Knowledge Award King Faisal International Prize in Medicine |
| Scientific career | |
| Fields | Physiology Biochemistry |
| Institutions | Jackson Laboratory |
| Thesis | Studies on the saturation of sterols by intestinal bacteria (1958) |
| Doctoral advisor | Carl August Baumann |
Douglas L. Coleman (October 6, 1931 - April 16, 2014) was a scientist andprofessoremeritus at theJackson Laboratory, inBar Harbor,Maine. His work predicted that there exists ahormone that can cause mice to feelfull, and that amutation in thegene encoding this hormone can lead to obesity.[3] The gene and corresponding hormone were discovered about 20 years later byJeffrey M. Friedman,Rudolph Leibel, and their research teams atRockefeller University, which Friedman namedleptin.[4]
Coleman was born inStratford,Ontario,Canada in 1931. He was the first in his family to finishhigh school.[5] He obtained hisBSc fromMcMaster University in 1954. At the encouragement of abiochemistry professor at McMaster,[3] Coleman attended theUniversity of Wisconsin–Madison for aPhD, which he obtained in 1958.
After receiving hisPhD, Coleman did not continue in academia or entered the industry, as was common at the time. Instead, he became an associate staff scientist at the Roscoe B. Jackson Memorial Laboratory (nowJackson Laboratory) inBar Harbor,Maine.[6] Initially planning to stay one to two years, Coleman ended up spending his entire career at the Jackson Laboratory.[7]
He was promoted to a staff scientist at Jackson Laboratory in 1961 and became a senior staff scientist in 1968. He was the assistant director of research from 1968 to 1970 and interim director between 1975 and 1976.[2]
Coleman retired in 1991[7] at the age of 62.[8]
Before Coleman's experiments, there was evidence that thehypothalamus was a master regulator ofenergy balance by responding to a factor that traveled inblood.[4][9] When Coleman joined theJackson Laboratory, only oneobesemouse strain existed. This strain contained amutation, calledob (for obese), at both copies of theDNA atchromosome 6, and so was designatedob/ob.[3]
In 1966, Coleman and his colleagues reported a second obese mouse strain that looked very similar toob/ob mice but had another mutation. The mutation occurred inchromosome 4 and was calleddb (for diabetes).[10] A major difference between the two strains was that thedb/db mice had severe diabetes while theob/ob mice only mild diabetes. Importantly, only mice that werehomozygous with theob ordb mutation (meaning they had the mutation at both copies of the DNA) were obese. This meant in these two strains, obesity was anautosomal recessive trait.
Coleman wondered if there existed a biological molecule that caused obesity and was produced in adb/db but not normal mice, or, conversely, if there existed a molecule that prevented obesity in normal mice. Aware of previousparabiosis experiments by William Hervey from theUniversity of Cambridge, who surgically joined theblood vessels of normalrats with rats that had injuries at the hypothalamus, Coleman performed similar experiments on normal,ob/ob anddb/db mice. He first joineddb/db mice to normal ones, and found that normal mice dramatically ate less, had a large decrease inplasma glucose andinsulin levels, and eventually died, whiledb/db mice were unaffected and kept gainingfat and weight.[11]
He then joinedob/ob mice with normal mice, and observed a completely different scenario: normal mice had no changes butob/ob mice ate less and lost weight. When Coleman ended the union,ob/ob mice gained weight and became obese again. Lastly, whenob/ob anddb/db mice were surgically joined together,db/db mice kept gaining weight whereasob/ob mice significantly reduced theirfood intake and weight and died.[12]
His findings led Coleman to conclude thatob/ob mice lacked acirculating factor that regulates food intake and weight, and thatdb/db mice overproduced this factor but could not respond to it. Whendb/db mice was joined toob/ob or normal mice, however, this factor traveled throughblood to the other mouse and reduced theireating and weight.[13] Connecting these results to contemporary understanding, he also hypothesized that the hypothalamus contained the area that responded to the circulating factor.
About 20 years later, thegenes whereob anddb mutations occurred were identified byJeffrey M. Friedman,Rudolph Leibel (both fromRockefeller University) andLouis Tartaglia (fromMillennium Pharmaceuticals, now acquired byTakeda Pharmaceutical Company and renamedTakeda Oncology).[4] Theob gene is now known asLEP and theproteinhormone it encodesleptin, a name that Friedman coined. Thedb gene has been confirmed to be areceptor for the leptin protein, and was renamedLEPR.[14]
Coleman met his wife, Beverly J. Benallick, during hisundergraduate years atMcMaster University, where Benallick was the only femalechemistry major at the time.[5] Benallick passed away in 2009.[15]
After retirement, Coleman was involved inforest management, land protection, and nature conservation. He created recreational trails in his 20-hectarewoodland for the public and especially students, and also helped his wife found a wildlife garden for people not able to walk the woodland. He was a director and president of theFrenchman Bay Conservancy, and a longtime member of theLamoine Planning Board.[2]
He established twoUSD $100,000 funds at theJackson Laboratory: the Douglas Coleman Research Fund to support early-career scientists studyingobesity anddiabetes, and the Beverly Coleman Memorial Fund to support young students and educational programmes.[2]
Coleman died inLamoine,Maine on April 16, 2014.[16][17]
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