Gene linking stress to obesity, diabetes discovered

Weizmann Institute scientists identify a single gene related to metabolic changes which can lead to all three phenomena.

By JUDY SIEGEL
April 21, 2010 07:37
2 minute read.
A cell

body cell 311. (photo credit: Courtesy)

 
X

Dear Reader,
As you can imagine, more people are reading The Jerusalem Post than ever before. Nevertheless, traditional business models are no longer sustainable and high-quality publications, like ours, are being forced to look for new ways to keep going. Unlike many other news organizations, we have not put up a paywall. We want to keep our journalism open and accessible and be able to keep providing you with news and analysis from the frontlines of Israel, the Middle East and the Jewish World.

As one of our loyal readers, we ask you to be our partner.

For $5 a month you will receive access to the following:

  • A user experience almost completely free of ads
  • Access to our Premium Section
  • Content from the award-winning Jerusalem Report and our monthly magazine to learn Hebrew - Ivrit
  • A brand new ePaper featuring the daily newspaper as it appears in print in Israel

Help us grow and continue telling Israel’s story to the world.

Thank you,

Ronit Hasin-Hochman, CEO, Jerusalem Post Group
Yaakov Katz, Editor-in-Chief

UPGRADE YOUR JPOST EXPERIENCE FOR 5$ PER MONTH Show me later

Changes in the activity of a single gene in the brain can lead to metabolic changes that cause mice to develop symptoms associated with type 2 diabetes, as well as trigger anxious behavior.

These findings, discovered by Weizmann Institute of Science researchers, were published online this week in the Proceedings of the National Academy of Sciences (PNAS).

The constant stress many are exposed to in our modern society may thus be taking a heavy toll: Anxiety disorders and depression, as well as metabolic disorders such as obesity, type 2 diabetes and arteriosclerosis, have all been linked to stress.

These problems are reaching epidemic proportions. Type 2 diabetes alone is expected to affect some 360 million people around the world in 20 years.

The connection between stress, changes in appetite and anxiety-related behavior was recently proven scientifically, but the exact reasons for this were not clear until Dr. Alon Chen of the Rehovot institute’s neurobiology department and colleagues made their gene discovery.

They found that all the body’s systems are involved in the stress response, which evolved to deal with threats and danger. Behavioral changes tied to stress include heightened anxiety and concentration, while other changes in the body include heat-generation, changes in the metabolism of various substances and even changes in food preferences.

The Weizmann team suspected that a protein known as Urocortin-3 (Ucn3) was involved in tying all of these together. Produced in certain brain cells – especially in times of stress – it is known to play a role in regulating the body’s stress response.

These nerve cells have extensions that act as “highways” to speed Ucn3 on to two other sites in the brain: One, in the hypothalamus – the brain’s center for hormonal regulation of basic bodily functions – oversees, among other things, substance exchange and feelings of hunger and satiety; the other is involved in regulating behavior, including anxiety levels.


Nerve cells in both these areas have special receptors for Ucn3 on their surfaces, and the protein binds to these receptors to initiate the stress response.

The researchers developed a new, finely tuned method for influencing the activity of a single gene in one area in the brain, using it to increase the amounts of Ucn3 produced in just that location.

They found that heightened levels of the protein produced two different effects: The mice’s anxiety-related behavior increased, and their bodies also underwent metabolic changes. With excess Ucn3, their bodies burned more sugar and fewer fatty acids, and their metabolic rate sped up.

These mice began to show signs of the first stages of type 2 diabetes: A drop in muscle sensitivity to insulin delayed sugar uptake by the cells, resulting in raised sugar levels in the blood. The pancreas then produced extra insulin to make up for the perceived “deficit.”

“We showed that the actions of single gene in just one part of the brain can have profound effects on the metabolism of the whole body,” says Chen.

This mechanism, which appears to be a “smoking gun” tying stress levels to metabolic disease, might, in the future, point the way toward the treatment or prevention of a number of stress-related diseases.

Join Jerusalem Post Premium Plus now for just $5 and upgrade your experience with an ads-free website and exclusive content. Click here>>

Related Content

[illustrative photo]
September 24, 2011
Diabetes may significantly increase risk of dementia

By UNIVERSITY OF MICHIGAN HEALTH SYSTEM