How Sweet It Isn't: Hormone Dampens Taste for Sugary Foods

From the WebMD Archives

Sept. 18, 2000 -- That fat little mouse nibbling on cookies in your pantry may not be able to help himself: Japanese researchers have discovered that mice whose bodies lack the ability to use a naturally occurring fat-fighting hormone have a real sweet tooth. The finding, published in the journal Proceedings of the National Academy of Sciences, could help explain why some obese people can't resist sugary foods.

On the other hand, the researchers found that normal mice lose their fondness for sugar when injected with this so-called obesity hormone, called leptin. The shot did not appear to change their abilities to taste the other basic tastes of sour, salty, and bitter.

This finding suggests that the hormone may act on taste-sensitive cells in the tongue to suppress cravings for sweet stuff. The finding also may shed more light on the causes of obesity, the study's authors propose.

Leptin, a protein produced by fat cells in the body, has been shown to both reduce food intake and increase energy use by acting on a part of the brain known as the hypothalamus. Earlier studies have shown that extremely obese mice that have been bred to have diabetes appear to be particularly sensitive to sweet tastes such as sugar and saccharin, and they show a marked preference for sugary foods when compared with their normal-sized cousins. These obese mice also have fewer receptors, or docking sites, for leptin on their cells and thus are less susceptible to its effects than normal mice.

The Japanese researchers suspected that the gene that makes leptin could somehow be related to leptin receptors, which could explain why the mice seemed to prefer sweets. To test this idea, they measured how the nervous systems of both diabetic and normal mice responded to various tastes, both before and after injections of leptin.

They found that the skinny mice appeared to lose their sensitivity to sugar or saccharin after a leptin injection, while the diabetic mice seemed to have no change in taste sensitivity.

But whether what's true in mice will be true in men is another question, two leptin researchers tell WebMD.


"I think it's interesting in that it's another demonstration that leptin may have actions outside of the hypothalamus," says Joel Keith Elmquist PhD, DVM. Elmquist is in the division of endocrinology at Beth Israel-Deaconess Medical Center and is an assistant professor of neurology at Harvard Medical School in Boston.

He adds that a true abnormality in the receptors for leptin is rare in humans, but it's thought that we can have what's called leptin resistance. This phenomenon can be compared with memory loss -- the object is still there, but you don't recognize it. In this case, the body has normal, or even elevated, amounts of leptin, but the cells that need leptin to control food intake or increase energy use no longer recognize it.

"So a lack of response to leptin is thought to very strongly contribute to obesity. Perhaps [that] resistance [occurs] at the level of the taste system as well, [and that] may contribute to ... obesity," Elmquist tells WebMD.

Another Boston-based researcher is less sure.

"Many people [have] ... high leptin levels already, and in human studies of the effect of leptin on weight loss, some people lose weight but many people don't," says Andrew Greenberg, MD, director of the program in obesity and metabolism at the Jean Mayer USDA Human Nutrition Research Center at Tufts University.

Greenberg suggests that although the study's findings are interesting, the exact role of leptin in causing obesity is still unclear. " "Leptin has so many effects; humans who have no leptin, for example, eat lots and lots of food. This may be one piece of the puzzle, but it's probably not a major piece," he tells WebMD.


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