Genes and Obesity

Gretchen Becker Health Guide
  • One of the difficult things about being obese is that most of society assumes it’s because you’re a lazy glutton.

     

    Sometimes people do gain weight because they overeat as a result of psychological problems, like the man who weighed 980 pounds but recently lost more than 336 pounds and is still obese, carrying around about 100 pounds of excess skin. He was abused as a child by his father and a female relative but kept it all inside him and used food to cover up the hurt.

     

    But in other cases, people gain weight because there’s some fault in their metabolic control. The most clearcut example of this is leptin deficiency, found in a tiny number of people worldwide. But with leptin injections, the patients eat normally and lose weight without trying.

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    Most overweight people are somewhere between these two extremes, with different amounts of genetic defects and psychological challenges.

     

    Every now and then, someone will report that some genetic manipulation in mice seems to protect the mice from obesity. Such is the case in an interesting study on fat storage recently reported in Nature Medicine.

     

    Researchers at the Joslin Diabetes Center reported that mice lacking a particular “transcriptional co-regulator” called TRIP-Br2 were resistant to obesity, no matter what they ate. Transcription factors control which genes are expressed, and the genes affected by TRIP-Br2 are involved with fat storage, breakdown, and use for energy.

     

    In the mice without TRIP-Br2, any fat in the fat cells was broken down at a high rate into free fatty acids, which were then burned for energy. Thus these mice could eat a high-fat diet and, unlike the control mice given a high-fat diet, remain lean. These mice also had less insulin resistance and better glucose tolerance.

     

    So having TRIP-Br2 makes you fatter and more insulin resistant.

     

    Although mouse studies often don’t translate into humans, the researchers found that TRIP-Br2 was elevated in the visceral fat of obese humans, which suggests that perhaps the same factors do work in humans.

     

    So far, these findings have no practical application, although the researchers are seeking a drug that would inhibit TRIP-Br2. Finding such a drug is not apt to happen in the near future, however.

     

    Nevertheless, I think knowing that it’s possible for some genetic difference to let some people eat all they want and remain thin, like the mice missing TRIP-Br2, while others must watch every calorie is useful in reducing the guilt that overweight people often feel when the media constantly talks about the “obesity epidemic” as if it’s caused by gorging on fast food.

     

     

     

     

Published On: February 07, 2013