Scientists Discover New Mechanism For Controlling Blood Sugar Level

Main Category: Diabetes
Article Date: 30 Nov 2010 - 0:00 PST window.fbAsyncInit = function() { FB.init({ appId: 'aa16a4bf93f23f07eb33109d5f1134d3', status: true, cookie: true, xfbml: true, channelUrl: 'http://www.medicalnewstoday.com/scripts/facebooklike.html'}); }; (function() { var e = document.createElement('script'); e.async = true; e.src = document.location.protocol + '//connect.facebook.net/en_US/all.js'; document.getElementById('fb-root').appendChild(e); }()); email to a friend ? printer friendly ? opinions ?

Medical scientists at the University of Leicester have identified for the first time a new way in which our body controls the levels of sugar in our blood following a meal.

They have discovered the part played by a particular protein in helping to maintain correct blood sugar levels.

The breakthrough was made in the University of Leicester by a team led by Professor Andrew Tobin, Professor of Cell Biology, who is a Wellcome Trust Senior Research Fellow. The research is published online ahead of print in the prestigious international scientific journal the Proceedings of the National Academy of Sciences.

Professor Tobin said: "The work, which was done wholly at the University of Leicester, is focused on the mechanisms by which our bodies control the level of sugar in our blood following a meal.

"We found that in order to maintain the correct levels of sugar, a protein present on the cells that release insulin in the pancreas has to be active. This protein, called the M3-muscarinic receptor, is not only active but also needs to undergo a specific change. This change triggers insulin release and the control of blood sugar levels."

Professor Tobin added: "Without the change in the M3-muscarinic receptor protein sugar levels go up in the same way that we see in diabetes. We are of course testing if the mechanism of controlling sugar levels we have discovered is one of the mechanisms disrupted in diabetes. If this were the case then our studies would have important implications in diabetes."

The paper was authored by:

Kok Choi Kong, Adrian J. Butcher, Phillip McWilliams, David Jones, Sarah E. Munson, Hannah A. Cragg, Alison D. Smart and Andrew B. Tobin at the University of Leicester, Jurgen Wess at the National Institutes of Health, Fadi F. Hamdan at the University of Montreal, Tim Werry at the GlaxoSmithKline, and Elizabeth M. Rosethorne, Steven J. Charlton at Novartis Institutes for Biomedical Research.

The work was funded by the Wellcome Trust.

Note

M3-muscarinic receptor promotes insulin release via receptor phosphorylation/arrestin-dependent activation of protein kinase D1 appeared in the Proceedings of the National Academy of Sciences (PNAS).

Source:
University of Leicester
Wellcome Trust

Please rate this article:
(Hover over the stars
then click to rate)

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

posted by Nelson Philips on 30 Nov 2010 at 4:44 am

I am interested in this new breakthrough in blood sugar control.

| post followup | alert a moderator |

All opinions are moderated before being added.

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

View the original article here

Understanding diabetes at the molecular level

ScienceDaily (Nov. 8, 2010) ? United States and Japanese researchers have identified a key step in metabolic pathways linked to diabetes and cancer. The study on activation of the protein complex TORC 2 was published online in the journal Current Biology Oct. 28.

TORC 2 activates a protein called Akt, which plays a crucial role in how cells respond to insulin, said Kazuo Shiozaki, professor of microbiology in the College of Biological Sciences at UC Davis and senior author on the paper.

Normally, insulin triggers fat and muscle cells to take up sugar from the blood. Patients with type II diabetes make plenty of insulin, but their cells do not respond to it properly. Akt plays a role in the series of steps between insulin exposure and sugar uptake; specifically, it causes proteins that take sugar from the blood to move to the cell surface. Mice that lack the gene for Akt develop diabetes-like symptoms.

"We know that Akt is a key player in diabetes, so we are trying to work upstream from there," Shiozaki said.

Akt also controls cell growth in early embryos and can promote the growth of cancer cells, he added.

Since TORC 2 was first identified in 2005 as a regulator of Akt, researchers have been trying to identify how it is activated, Shiozaki said. The complex appears to be very similar across organisms ranging from humans to yeast.

Shiozaki and colleagues Hisashi Tatebe, Susumu Morigasaki, Shinichi Murayama and Cui Tracy Zeng studied TORC 2 in a yeast. They found that a protein called Ryh1, when bound to another molecule called guanosine triphosphate, is needed to activate TORC 2.

Yeast strains that had a defective form of Ryh1 were more sensitive to temperature or other stressful conditions.

Ryh1 is very similar to a human protein, Rab6. The researchers found that human Rab6 could to some extent replace yeast Ryh1 as an activator of TORC 2 in defective yeast strains.

Rab6 belongs to a class of proteins better known for moving other proteins around within cells. This suggests that Rab6 might play a dual role in insulin signaling, Shiozaki said.

"Our discovery suggests that the early and late steps in insulin response are closely linked to each other," Shiozaki said.

Co-authors Tatebe, Morigasaki and Murayama also hold positions at the Nara Institute of Science and Technology, Japan. The work was funded by grants from the National Institutes of Health, the University of California Cancer Research Coordinating Committee, and the Japan Society for the Promotion of Science. Morigasaki is an international research fellow of the Nara Institute of Science and Technology Global Center of Excellence Program, funded by the Ministry of Education, Culture, Sports, Science and Technology of Japan.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of California - Davis, via EurekAlert!, a service of AAAS.

Journal Reference:

Hisashi Tatebe, Susumu Morigasaki, Shinichi Murayama, Cui Tracy Zeng, Kazuhiro Shiozaki. Rab-Family GTPase Regulates TOR Complex 2 Signaling in Fission Yeast. Current Biology, 2010; DOI: 10.1016/j.cub.2010.10.026

Note: If no author is given, the source is cited instead.

View the original article here