How we can stop stress from making us obese

Contact: Dr. Branwen Morgan
b.morgan@garvan.org.au
61-043-407-1326
Research Australia

Professor Herbert Herzog, Director of the Neuroscience Research Program at the Garvan Institute of Medical Research, together with scientists from the US and Slovakia, have shown that neuropeptide Y (NPY), a molecule the body releases when stressed, can ‘unlock’ Y2 receptors in the body’s fat cells, stimulating the cells to grow in size and number. By blocking those receptors, it may be possible to prevent fat growth, or make fat cells die.

“We have known for over a decade that there is a connection between chronic stress and obesity,” said Professor Herzog. “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.”

“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).”

“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.”

Scientists at Georgetown University (Washington D.C), part of this collaborative study, have found a direct connection between stress, a high calorie diet and unexpectedly high weight gain. Stressed and unstressed mice were fed normal diets and high calorie (high fat and high sugar, or so called ‘comfort food’) diets. The mice on normal diets did not become obese. However, stressed mice on high calorie diets gained twice as much fat as unstressed mice on the same diet. The novel and unexpected finding was that 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,” says senior author of the Nature Medicine paper, Professor Zofia Zukowska of Georgetown University. “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 believes that these research findings will 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.”

“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.”

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Notes to editors:

Stress-activated adipogenic pathway in fat tissue exaggerates diet-induced obesity and metabolic syndrome.
Kuo, L.E., Kitlinska, J.B., Tilan, J.U., Li, L., Baker, S.B., Johnson, M.D., Lee, E.W., Burnett, M.S., Fricke, S.T., Kvetnansky, R.K., Herzog, H. & Zukowska, Z.
Nature Medicine advance online publication, 1 July 2007

The study was co-funded by the National Institutes of Health, the American Heart Association, and the Slovak Research and Development Agency.

ABOUT GARVAN

The Garvan Institute of Medical Research was founded in 1963. Initially a research department of St Vincent’s Hospital in Sydney, it is now one of Australia’s largest medical research institutions with approximately 400 scientists, students and support staff. Garvan’s main research programs are: Cancer, Diabetes & Obesity, Arthritis & Immunology, Osteoporosis, and Neuroscience. The Garvan’s mission is to make significant contributions to medical science that will change the directions of science and medicine and have major impacts on human health. The outcome of Garvan’s discoveries is the development of better methods of diagnosis, treatment, and ultimately, prevention of disease.

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How to lose weight and not go hungry: HU researcher develops drug that mimics feeling of ‘fullness’

Contact: Jerry Barach
jerryb@savion.huji.ac.il
972-258-82904
The Hebrew University of Jerusalem

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Yaniv Linde in his lab.

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Jerusalem, June 6, 2007 — Millions of people the world over suffer today from obesity, yet there is no “magic bullet” that has yet provided a universally accepted solution. However, a young researcher at the Hebrew University of Jerusalem feels he has come up with a practical weight loss solution for the obese person without his having to feel hungry.

For this development, Yaniv Linde, a 32-year-old Ph.D. student of Prof. Chaim Gilon in the Department of Organic Chemistry at the Hebrew University, has been named a first place winner of a Kaye Innovation Award, which was presented today (June 6) during the 70th meeting of the Hebrew University Board of Governors.

Linde and his associates have developed a compound that mimics the activity of the naturally occurring hormone called aMSH. This hormone is naturally excreted during eating and binds to a receptor in the brain called MC4R. When this “communication” occurs on a substantial level, the brain sends out a signal that one feels “full.”

The young Hebrew university researchers developed a novel method for synthesizing a peptide (a peptide is a compound linking two or more amino acids) which can serve as an analog to the naturally occurring aMSH hormone. They were able to demonstrate that their peptide, which they call BL-3020, displayed good metabolic stability to intestinal enzymes when swallowed, and that it was able to cross the intestinal wall and gain access into the blood stream. Once in the blood, it could make its way to the MC4R receptor and “close the circuit” to send out the “full” signal.

The result is that a person seriously wishing to overcome obesity could take this compound orally in order to curb his appetite, thus leading to natural weight loss. In experiments with mice, it was shown that a single oral administration of BL-3020 led to reduced consumption over a period of 24 hours. Over a 12-day period of daily dosages, the mice weighed 40 percent less than the average for mice of their size and age who were not being given the compound.

The peptide has been patented in Europe and the U.S., and a commercial firm, Bioline RX Ltd. of Jerusalem has purchased development rights from Yissum, the Hebrew University’s technology transfer company, and is currently working towards creating a commercial anti-obesity drug.

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The Kaye Innovation Awards at the Hebrew University have been awarded annually since 1994. Isaac Kaye of England, a prominent industrialist in the pharmaceutical industry, established the awards to encourage faculty, staff, and students of the Hebrew University to develop innovative methods and inventions with good commercial potential which will benefit the university and society.

For further information:
Jerry Barach, Dept. of Media Relations, the Hebrew University, Tel: 02-588-2904, or Orit Sulitzeanu, Hebrew University spokesperson, Tel: 02-5882910 or 052-260-8016.
Internet site: http://media.huji.ac.il.

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