Boffins find pathway behind stress-triggered obesity

Scientists conducting a collaborative study have identified the chain of molecular events that links chronic stress with obesity.

London, July 2 : Scientists conducting a collaborative study have identified the chain of molecular events that links chronic stress with obesity.

Professor Herbert Herzog, Director of the Neuroscience Research Program at the Garvan Institute of Medical Research, says that neuropeptide Y (NPY), a molecule that the body releases when stressed, can 'unlock' Y2 receptors in the body's fat cells, stimulating the cells to grow in size and number.

He suggests that by inactivating these receptors the growth of fat cells may be prevented.

"We have known for over a decade that there is a connection between chronic stress and obesity," Nature Medicine quoted Professor Herzog, who conducted the collaborative study with colleagues from the US and Slovakia, as saying.

"We also know that NPY plays a major role in other chronic stress-induced conditions, such as susceptibility to infection. Now we have identified the exact pathway, or chain of molecular events, that links chronic stress with obesity," he added.

He also says that timely intervention to stop NPY from causing fat to amass may also be helpful in cutting the risk of various other serious diseases.

"There is not much we can do about the increased levels of NPY caused by stress, but we can do something about the damage it causes. If we can interfere before it causes fat to amass, it could have a major impact on cardiovascular disease, diabetes, and cancer (which all have links with obesity)," Professor Herzog said.

"Basically, when we have a stress reaction, NPY levels rise in our bodies, causing our heart rate and blood pressure to go up, among other things. Stress reactions are normal, unavoidable, and generally serve a useful purpose in life. It's when stress is chronic that its effects become damaging," he added.

During the course of study, collaborators from Georgetown University found a direct connection between stress, a high calorie diet, and unexpectedly high weight gain. They fed stressed and unstressed mice on normal diets and high calorie diets.

It was found that none of the animals on normal diets became obese. But stressed mice on high calorie diets had gained twice as much fat as unstressed animals on the same diet.

The researchers noted when stressed and non-stressed animals ate the same high calorie foods, the stressed animals utilised and stored fat differently.

"Our findings suggest that we may be able to reverse or prevent obesity caused by stress and diet, including the worst kind of obesity; the apple-shaped type, which makes people more susceptible to heart disease and diabetes," said senior author of the paper, Professor Zofia Zukowska.

"Using animal models, in which we have either blocked the Y2 receptor, or selectively removed the gene from the abdominal fat cells, we have shown that stressed mice on high calorie diets do not become obese. Even more surprisingly, in addition to having flatter bellies, adverse metabolic changes linked to stress and diet, which include glucose intolerance and fatty liver, became markedly reduced. We do not know yet exactly how that happens, but the effect was remarkable," she said.

Professor Herzog reckons that the new findings may have a profound effect on the way society will deal with the obesity epidemic.

"There are millions of people around the world who have lived with high levels of stress for so long their bodies think it's 'normal'. If these people also eat a high fat and high sugar diet, which is what many do as a way to reduce their stress, they will become obese," he said.

"Until now, the pharmaceutical industry has focused on appetite suppressants with only moderate success. Our hope is that in the near future pharmaceutical companies, using the results of our research, will develop antagonists against the Y2 receptor that will bring about a reduction in fat cells," he added.

ANI