Tuesday, 15 September 2015

New hope for Diabetes patients as stanford researchers moves closer to discovering the drug for type 1 diabetes.

Diabetes points Stanford scientists toward old gallstone drug.

A gallstone-related drug, already approved in Asia and Europe, could enter human clinical trials soon as an experimental way to block Type 1 diabetes before patients even develop symptoms.
In a paper published Monday in the Journal of Clinical Investigation, researchers at Stanford University and Seattle's Benaroya Research Institute at Virginia Mason Hospital said a study of the drug — called hymecromone — blocked production of a substance that is essential for the development of Type 1 diabetes. Although the study was in mice, they believe the drug ultimately could be used to stop a disease that afflicts one in 300 people in the United States.


Whether the experimental drug is able to wend its way through the multibillion-dollar, multi-year drug-approval process remains to be seen. But the study, funded by the Juvenile Diabetes Research Foundation and the National Institutes of Health, could lay the foundation for preventing millions of so-called pre-diabetics from joining the ranks of the 1.25 million Americans with Type 1 diabetes.


Type 1 diabetes, also known as juvenile diabetes, is an autoimmune disease, where the pancreas stops producing insulin, a hormone that converts sugars into energy. More common Type 2 diabetes, in contrast, is a metabolic disorder in which insulin still is produced but the body can't use it effectively.
The lab of Dr. Paul Bollyky a Stanford assistant professor of infectious diseases who led the team exploring hymecromone in Type 1 diabetes, is prepping a human clinical trial of the drug. It also has received preliminary funding from SPARK, a Stanford program designed to transform bench research into bedside drugs and diagnostics.
Beyond the commercial possibilities, hypercromone is exciting scientifically.
Early in Type 1 diabetes, scattered clusters of human pancreas cells, called islets, become inflamed when otherwise-protective immune cells attack. The attack eventually spreads to beta cells, halting the production of insulin.
By the time Type 1 diabetes can be identified, some 90 percent of pancreatic beta cells already have been killed off.

Ron Leuty, San Francisco BTs

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