Obesity Cause: Is It in the Brain?
Study Shows Cells in Brain May Be Linked to Eating Behavior
WebMD News Archive
Oct. 27, 2005 -- Obesity may be triggered by a certain type of cell in the brain, according to new research.
The study showed that when these cells, known as NPY/AgRP, were lacking in mice, the animals began to eat less and less. After 6-8 days the mice lost 20% of their body weight.
Researchers say the findings bring them one step closer to understanding the biological causes of obesity and what makes one person more prone to overeating than another.
The Brain's Role in Obesity
Previous studies have shown that a group of about 5,000 cells in a particular region of the brain are responsible for sorting out signals the body sends about when it's hungry or full.
Hormones, such as insulin, leptin, and ghrelin, deliver this information about whether the body needs more fuel to the brain, where it's processed by two types of cells -- POMC and NPY/AgRP.
POMC cells send signals to other parts of the brain to reduce appetite. For example, mice that lack POMC cells in the brain eat excessively.
But researchers say the role of NPY/AgRP cells -- which recognize and respond to hunger signals -- has been difficult to determine.
New Brain-Obesity Link Found
In the study, published in the journal Science, researchers looked at the influence of the NPY/AgRP cells on the eating behavior of mice.
Using new genetic technology, researchers eliminated NPY/AgRP cells in adult and infant mice and then monitored changes in how much they ate.
The results showed that eliminating NPY/AgRP in adult mice produced dramatic effects and rapid weight loss.
But if the cells were killed off when the mice were less than 8 days old the mice ate normally and maintained a normal body weight.
Researchers say the results suggest that if NPY/AgRP cells are eliminated early in life, animals find ways to compensate and maintain normal eating habits. The researchers say that brain cells may compensate by continuing to develop and by forming connections with other cells.
"I would predict that if you could do the experiment in humans, this result would be the same, because the circuits are the same," says researcher Richard D. Palmiter, an investigator at the Howard Hughes Medical Institute, in a news release.
Palmiter says mutations in human genes that affect the survival of these neurons or their ability to respond to hormonal hunger signals could alter eating behavior and natural body weight regulation.