{"id":10833,"date":"2017-06-07T01:51:11","date_gmt":"2017-06-07T01:51:11","guid":{"rendered":"http:\/\/magazines.uthscsa.edu\/mission-new\/?p=10833"},"modified":"2018-01-22T20:26:31","modified_gmt":"2018-01-22T20:26:31","slug":"no-more-shots","status":"publish","type":"post","link":"https:\/\/magazines.uthscsa.edu\/mission\/no-more-shots\/","title":{"rendered":"No more shots"},"content":{"rendered":"
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A potential cure for Type 1 diabetes is on the horizon, and the novel approach would also allow Type 2 diabetics to stop insulin shots.<\/figcaption><\/figure>\n

A potential cure for Type 1 diabetes is on the horizon, and the novel approach would also allow Type 2 diabetics to stop insulin shots.<\/p>\n

The discovery increases the types of pancreatic cells that secrete insulin.<\/p>\n

UT Health San Antonio researchers have a goal to reach human clinical trials in three years, but to do so they must first test the strategy in large-animal studies. Those studies will precede application to the Food and Drug Administration for Investigational New Drug approval, said Bruno Doiron, Ph.D., a co-inventor.<\/p>\n

The scientists received a U.S. patent in January, and UT Health San Antonio is spinning out a company to begin commercialization.<\/p>\n

The strategy has cured diabetes
\nin mice.<\/p>\n

\u201cIt worked perfectly,\u201d said Dr. Doiron, assistant professor of medicine. \u201cWe cured mice for one year without any side effects. But it\u2019s a mouse model, so caution is needed. We want to bring this to large animals that are closer to humans in physiology of the endocrine system.\u201d<\/p>\n

Ralph DeFronzo, M.D., professor of medicine and chief of the Division of Diabetes, is co-inventor on the patent. \u201cThe pancreas has many other cell types besides beta cells, and our approach is to alter these cells so that they start to secrete insulin, but only in response to glucose [sugar],\u201d he said. \u201cThis is basically just like beta cells.\u201d<\/p>\n

Insulin, which lowers blood sugar, is only made by beta cells. In Type 1 diabetes, beta cells are destroyed by the immune system and the person has no insulin. In Type 2 diabetes, beta cells fail and insulin decreases. At the same time in Type 2, the body doesn\u2019t use insulin efficiently.<\/p>\n

The therapy is accomplished by a technique called gene transfer. A virus is used as a vector, or carrier, to introduce selected genes into the pancreas. These genes become incorporated and cause digestive enzymes and other cell types to make insulin.<\/p>\n

Gene transfer using a viral vector has been approved nearly 50 times by the FDA to treat various diseases, Dr. DeFronzo said. It is proven in treating rare childhood diseases, and good manufacturing processes ensure safety.<\/p>\n

Unlike beta cells, which the body rejects in Type 1 diabetes, the other cell populations of the pancreas co-exist with the body\u2019s immune defenses.<\/p>\n

\u201cIf a Type 1 diabetic has been living with these cells for 30, 40 or 50 years, and all we\u2019re getting them to do is secrete insulin, we expect there to be no adverse immune response,\u201d Dr. DeFronzo said.<\/p>\n

The therapy precisely regulates blood sugar in mice. This could be a major advance over traditional insulin therapy and some diabetes medications that drop blood sugar too low if not closely monitored.<\/p>\n

\u201cA major problem we have in the field of Type 1 diabetes is hypoglycemia [low blood sugar],\u201d Dr. Doiron said. \u201cThe gene transfer we propose is remarkable because the altered cells match the characteristics of beta cells. Insulin is only released in response to glucose.\u201d<\/p>\n

People don\u2019t have symptoms of diabetes until they have lost at least 80 percent of their beta cells, Dr. Doiron said.<\/p>\n

\u201cWe don\u2019t need to replicate all of the insulin-making function of beta cells,\u201d he said. \u201cOnly 20 percent restoration of this capacity is sufficient for a cure of Type 1.\u201d<\/p>\n","protected":false},"excerpt":{"rendered":"

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