Thursday, October 8, 2015

Newly Identified Biochemical Pathway Could Be Target for Insulin Control





This feels like we may be getting close to a solution for type 2 diabetes.  That is the monkey stalking all of us who live a modern life.  Old Age is not pleasant if you are fighting this.


I personally know several diabetes victims  and it is difficult to share actionable advice that helps a lot.  Yet by the time you have a problem that it identifiable, you are already suffering severe damage to your circulatory system that sends you down the road to ruin.


I have found though that the best actionable dietary step is to fold cabbage soup into your daily regime as a staple.  One friend reports that he is taking up four bowls per day and his diet is generally improving as well.  To that i have added canned Jerusalem artichokes as well.  He is encouraged because his energy levels have risen.

 
At least he acted. 


Newly Identified Biochemical Pathway Could Be Target for Insulin Control
Released: 21-Sep-2015 10:05 AM EDT

http://www.newswise.com/articles/view/640139/?sc=dwhn

Contact Information Available for logged-in reporters only
Citations Cell Reports; DK046492-22; K01GM109320-02; MOP 244739 


Newswise — DURHAM, N.C. – In the final event leading to the development of Type 2 diabetes, the pancreas loses its ability to secrete insulin and clear glucose from the blood. Preventing this breakdown in insulin secretion is a key goal in the fight to reduce the burden of a disease that afflicts an estimated 29 million people in the United States. 

Now researchers at Duke Medicine and the University of Alberta are reporting the identification of a new biochemical pathway to control insulin secretion from islet beta cells in the pancreas, establishing a potential target for insulin control.

The study, published online Sept. 24 in the journal Cell Reports, results from a field of work called metabolomics, which uses mass spectrometry instruments to measure and trace intermediate molecules in key metabolic pathways of cells and tissues. 

“The Duke group focused on metabolites in islet cells that changed in response to elevated external glucose concentrations,” said co-senior author Christopher B. Newgard, Ph.D., director of the Sarah W. Stedman Nutrition and Metabolism Center and the Duke Molecular Physiology Institute. “We found a strong increase in an intermediate in the purine/nucleotide metabolic pathway -- known as adenylosuccinate, or S-AMP -- in islets stimulated with glucose.”

Impairment of S-AMP production was shown to interfere with normal glucose-stimulated insulin secretion. The Duke and University of Alberta Diabetes Institute teams were also able to demonstrate that S-AMP is capable of rescuing impaired insulin secretion in islets from people with Type 2 diabetes. 

Newgard said the collaborative effort between the Duke and Alberta teams also yielded a separate finding, reported online Sept. 21 in the Journal of Clinical Investigation, which describes another molecular pathway that could be a potential metabolic target for insulin control.

In that study, the research teams identified a process that works essentially like a dimmer switch to adjust how much or how little insulin is secreted when blood sugar increases. This dimmer switch appears to be broken in Type 2 diabetes, but the researchers found that its function can be restored.

“For the moment, we have two separate mechanisms, but with further study we may find that they are more connected,” Newgard said. “Whether they are independent, additive or synergistic is unknown, so we are eager to bring the two projects together to see where that may lead.”

In addition to Newgard, study authors from Duke include Jessica R. Gooding; Mette V. Jensen; Brett R. Wenner; Danhong Lu; and Ramamani Arumugam.

Patrick E. MacDonald, Ph.D., of the Alberta Diabetes Institute, led the work at the University of Alberta, along with Xiaoqing Dai and Mourad Ferdaoussi.\

The National Institutes of Health (DK046492-22 and K01GM109320-02) and the Canadian Institutes of Health Research (MOP 244739) funded the research.

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