The Scientist : Hunger protein links stress, obesity
Hunger protein links stress, obesity
Neuropeptide Y builds fat when high-calorie diet combines with stress
[Published 2nd July 2007 10:14 AM GMT]
A neurotransmitter that acts as a central controller for appetite also regulates stress-induced obesity in the body's periphery, according to a paper in this month's Nature Medicine. The authors found that abdominal fat increased in stressed mice through the actions of neuropeptide Y (NPY) and one of its receptors. Blocking this receptor's signaling prevented stress-induced obesity.
"It's really quite an important study, both from a basic point of view as well as for potential clinical applications," said Esther Sabban of New York Medical College in Valhalla, who was not involved in the work.
Previous work has found that stress stimulates NPY release from sympathetic nerves. NPY activity also promotes obesity through central mechanisms, primarily by increasing appetite, senior author Zofia Zukowska of Georgetown University Medical Center in Washington, D.C., told The Scientist. However, NPY's "peripheral role has really never been studied," she said.
Zukowska's lab previously discovered that NPY promotes blood vessel growth through one of its receptors, NPY2R. So she and her colleagues suspected that NPY might control peripheral fat development by building blood vessels to feed fat cells.
Led by Lydia E. Kuo, also of Georgetown, the researchers found that NPY cultured with adipose tissue stimulated the proliferation and differentiation of fat cells. They blocked both of these effects with an NPY2R antagonist. The researchers also found that injecting NPY under the abdominal skin led to 50% increased adipose tissue in both obese and lean mice, while injecting the NPY2R antagonist decreased fat tissue by 50%. This antagonist also caused blood vessel atrophy in the abdominal fat, as expected from the researchers' previous work.
Since the NPY2R antagonist blocks development of both fat cells and blood vessels, it's "preventing the growth of abdominal fat by two similar but distinct mechanisms," said Markus Heilig, clinical director of the National Institute on Alcohol Abuse and Alcoholism in Bethesda, Md., who studies NPY signaling and was not involved in the work.
The authors next found that two weeks of daily exposure to a stressor -- either cold water baths or an aggressive mouse -- increased both NPY levels and abdominal fat deposits in mice fed a diet high in sugar and fat. Neither stress nor the high-calorie diet alone led to fat gain. Stress combined with the high-calorie diet also increased blood vessel development in abdominal fat tissue. NPY2R knockout mice, however, were resistant to stress-induced obesity.
I could be wrong on this, but I think they've found that body fat makes more NPY. So stress makes fat, and fat makes more stress and more fat. Vicious cycle.
Hunger protein links stress, obesity
Neuropeptide Y builds fat when high-calorie diet combines with stress
[Published 2nd July 2007 10:14 AM GMT]
A neurotransmitter that acts as a central controller for appetite also regulates stress-induced obesity in the body's periphery, according to a paper in this month's Nature Medicine. The authors found that abdominal fat increased in stressed mice through the actions of neuropeptide Y (NPY) and one of its receptors. Blocking this receptor's signaling prevented stress-induced obesity.
"It's really quite an important study, both from a basic point of view as well as for potential clinical applications," said Esther Sabban of New York Medical College in Valhalla, who was not involved in the work.
Previous work has found that stress stimulates NPY release from sympathetic nerves. NPY activity also promotes obesity through central mechanisms, primarily by increasing appetite, senior author Zofia Zukowska of Georgetown University Medical Center in Washington, D.C., told The Scientist. However, NPY's "peripheral role has really never been studied," she said.
Zukowska's lab previously discovered that NPY promotes blood vessel growth through one of its receptors, NPY2R. So she and her colleagues suspected that NPY might control peripheral fat development by building blood vessels to feed fat cells.
Led by Lydia E. Kuo, also of Georgetown, the researchers found that NPY cultured with adipose tissue stimulated the proliferation and differentiation of fat cells. They blocked both of these effects with an NPY2R antagonist. The researchers also found that injecting NPY under the abdominal skin led to 50% increased adipose tissue in both obese and lean mice, while injecting the NPY2R antagonist decreased fat tissue by 50%. This antagonist also caused blood vessel atrophy in the abdominal fat, as expected from the researchers' previous work.
Since the NPY2R antagonist blocks development of both fat cells and blood vessels, it's "preventing the growth of abdominal fat by two similar but distinct mechanisms," said Markus Heilig, clinical director of the National Institute on Alcohol Abuse and Alcoholism in Bethesda, Md., who studies NPY signaling and was not involved in the work.
The authors next found that two weeks of daily exposure to a stressor -- either cold water baths or an aggressive mouse -- increased both NPY levels and abdominal fat deposits in mice fed a diet high in sugar and fat. Neither stress nor the high-calorie diet alone led to fat gain. Stress combined with the high-calorie diet also increased blood vessel development in abdominal fat tissue. NPY2R knockout mice, however, were resistant to stress-induced obesity.
I could be wrong on this, but I think they've found that body fat makes more NPY. So stress makes fat, and fat makes more stress and more fat. Vicious cycle.
Comments