While the scientists rushed to call this an ““obesity gene,’’ it really appears to be more of a ““satiation gene.’’ Scientists think the gene sends a protein messenger to the brain, advising it that the body has stored enough fat. That’s a signal to stop eating. When the message isn’t sent, there’s no natural appetite suppressant – and no end to weight gain.
For years, researchers have hypothesized about a biochemical signal that helps keep eyes from becoming bigger than the proverbial stomach. ““Many investigators have been trying to find it,’’ says Dr. Jeffrey Friedman, who led the Rockefeller team. To date, five genes in mice have been implicated in some aspect of weight control. The newly discovered message sender seems particularly significant. When that gene mutates it no longer sends stop signals. And when that happens, the mice can grow three times fatter than normal.
Friedman and his colleagues then went looking for a human genetic counterpart. By comparing the mouse DNA with genes in human DNA, they were able to identify one that they believe could play a key role in regulating appetite. Friedman’s team doesn’t know yet whether variations in the gene are rare or common in humans – or whether they play a role in mild overweight as well as serious obesity. The next research step is to look for alterations in the human gene, and see if they correlate with obesity. ““There is a reasonable possibility that this will account for some, but by no means all, differences in body weight,’’ says Friedman. ““What’s exciting is that we’re now in a position to ask and answer these questions.''
It doesn’t take a geneticist to know that weight problems can be inherited. ““In the past we knew there was a genetic basis for obesity just by looking at patterns in families,’’ says Dr. Michael Hamilton, director of the Duke University Diet and Fitness Center. ““Now we have a gene we can identify, whose product affects our weight, and we can play with it.’’ It’s uncertain, though, what the practical effects of the new research will be. The lack of a genetic messenger may not relate to all types of obesity. And for humans, unlike mice, the problem does not lie entirely in the genes. Biology is only one fac-tor in why some people eat more than they need. ““These genetic discoveries will eventually show us who has the greatest propensity to gain weight,’’ says Kelly Brownell, director of the Yale University Center for Eating and Weight Disorders, ““but there are many paths to obesity.’’ For example: overeating to relieve stress, boredom or unhappiness.
Genetics also doesn’t explain why the incidence of obesity (20 percent or more over ideal weight) has grown from 25 percent of Americans to almost 35 percent in the past decade. ““Americans live in a toxic environment, where high-fat, high-calories foods are widely available and heavily promoted,’’ says Brownell. ““At the same time, opportunities for exercise decline. So whoever has the genetic tendency to be overweight is very likely to be so.’’ His solution: treat fattening, low-nutrient foods like potato chips the same as cigarettes, by taxing them heavily and making them socially unacceptable.
In the short run, last week’s news may at least help the self-esteem of some folks with abundant girth. Now, says Hamilton of Duke, ““Overweight people will feel somewhat reassured that obesity isn’t just a character flaw, the result of laziness or poor willpower.’’ But with obesity also linked to heart disease and other serious ailments, fighting fat has become a matter of life or death. Genetic research that could tip the scales in that struggle is worth its weight indeed.
Researchers think they’ve discovered some of the biological roots of obesity by studying mice. Here, step by step, is what they’ve found.
Three hungry mice start eating their dinners. They all consume the exact same portions, meeting their daily need for dietary fuel.
Two mice receive brain signals that their bodies have stored enough fat. The other has a mutated gene that doesn’t flash a “stop” message.
Knowing that they are full, the two mice leave. The other continues to eat. With time, the overeating mouse may grow three times fatter.
