|
About Diabetes
|
First of New Class of Drugs For Diabetes Shown
Successful Exenatide, the first of a new class of drugs for type 2
diabetes, was shown to reduce blood glucose (sugar) and body weight, and was
associated with improvement in markers of beta cell function, according to a
report here today at the American Diabetes Association's 64th Annual Scientific
Sessions. Based on the DCCT and UKPDS that assessed the impact of different levels of glucose control on diabetes complications, this magnitude of decline in A1C would be expected to be associated with significant reductions in the development of microvascular complications such as retinopathy, neuropathy and nephropathy,” said Dr. De Fronzo. Exenatide is the first new drug to emerge from exciting research into hormones in the gastrointestinal tract that affect diabetes and weight — generally known as gut hormones or incretin mimetics. A key hormone produced in the human gut is GLP-1, which can stimulate insulin production without causing the potentially threatening hypoglycemia (low blood sugar levels) associated with insulin injections and some oral anti-diabetes agents (such as sulfonylureas). Mounting evidence suggests that GLP-1 signaling regulates the proliferation of insulin-manufacturing islet cells in the pancreas, thus encouraging the body to make more insulin-producing beta cells. Exenatide is a synthetic version of exendin-4, a hormone in
the saliva of the Gila monster, a lizard native to several Southwestern American
states. It displays properties similar to human GLP-1. The lizard eats only four
times a year and turns its pancreas off the rest of the time. When it eats, it
secretes exendin-4 to turn its pancreas on again. “If continued research in humans duplicates all the results we have seen in animal studies — which have shown that exenatide causes the production of new insulin-producing beta cells — this would have major implications for the treatment of both type 1 and type 2 diabetes,” said Dr. DeFronzo. Source: Diabetes In Control.com: ADA 64th Scientific Sessions.
|