On April 16th, Douglas L. Coleman, one of the first supporters of genetic obesity, passed away. Coleman spent his life studying what makes certain mice obese and diabetic while other mice remain healthy despite a similar diet. In the 1990s his research culminated to the conclusion that a lack of the hormone leptin in the bloodstream led to obesity in both mice and humans. When fat cells build up in the body, they excrete leptin which helps the brain “feel” full. With this conclusion, Coleman made the claim that leptin deficiency will lead to obesity.
Interestingly enough, before his passing, Coleman found that there was in fact a small population of obese people with a leptin deficiency who he was able to treat and make thinner. On the other hand, most obese people have high levels of leptin in their blood, but for some reason are completely resistant to the “full” feeling that it creates.
Coleman’s research dominantly shows that leptin curbs hunger, but why are some people resistant? Current research is beginning to show that high levels of fructose may counteract the effects of leptin.
Although obesity may be genetic, what role do we have play in it? How much control do we have? How might this relate to the epigenome?
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