Glucokinase activators, new class of drugs for the treatment of type 2 diabetes .....

Glucokinase activators (GKAs) represent a promising new class of drugs for the treatment of type 2 diabetes that act directly on both the pancreas and the liver. Glucokinase (GK) is a key enzyme in glucose-sensing tissues that regulates glucose homeostatasis. GKAs lower glucose levels by enhancing the ability of pancreatic beta cells to “sense glucose” and increase insulin secretion in a glucose-dependent manner. Simultaneously, GKAs increase the uptake and disposal of glucose in the liver, while simultaneously reducing the amount it produces.

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Combination of Depagliflozin & Metaformin for type 2 diabatic ?

We knew that these two Depagliflozin (left) & Metaformin (right) compounds were being studied independently for type 2 diabetic condition. Dapagliflozin, an investigational compound, is a potential first-in-class SGLT2 inhibitor currently in Phase 3 trials under joint development as a once-daily oral therapy for the treatment of type 2 diabetes. SGLT2 inhibitors facilitate the elimination of glucose by the kidney, thereby returning serum glucose levels towards normal.

A recent study (24-week phase 3 clinical study by Bristol-Myers Squibb Company and AstraZeneca) demonstrated that the investigational drug dapagliflozin, added to metformin, demonstrated significant mean reductions in the primary endpoint, glycosylated hemoglobin level (HbA1c) and in the secondary endpoint, fasting plasma glucose (FPG) in patients with type 2 diabetes inadequately controlled with metformin alone, as compared to placebo plus metformin. Dapagliflozin is a novel, selective, sodium glucose co-transporter 2 (SGLT2) inhibitor.

The study also showed that individuals receiving dapagliflozin had statistically greater mean reductions in body weight compared to individuals taking placebo. Results from the 24-week study were presented at the 45th European Association for the Study of Diabetes Annual Meeting. This is the first public presentation of dapagliflozin Phase 3 data.

More interestingly, data on weight loss and blood pressure may be important adjuvants to glycemic control and is of great importance and hope in the days to come the SGLT2 inhibitors ( improved glycemic control) will play an important role in the type 2 diabetes. Given the continued rising prevalence of type 2 diabetes, there is an urgent need to have drugs of this kind..

Ref : http://www.astrazeneca.com/media/latest-press-releases/Dapagliflozen_Study014_EASD?itemId=7108139

New markers for early detection Of type 1 diabetes !

As per the claim by the lead researchers Prof. Dr. Anette Ziegler and Dr. Peter Achenbach, genetic factors play a significant role in the development of type 1 diabetes. The scientists were able to show that specific variants of the zinc transporter gene SLC30A8 influence the risk for diabetes. The body needs this gene in order to produce ZnT8. This protein influences the zinc transport into the beta cells and plays a crucial role in their maturation and thus also in insulin secretion.

Beta cells of the islets of Langerhans in the pancreas secrete the vitally important insulin. Already prior to the onset of type 1 diabetes the body’s own immune system destroys the beta cells. If this destruction exceeds a certain threshold, the disease becomes manifest: The insulin deficiency leads to various metabolic disturbances, including elevated blood glucose levels. Autoantibodies to ZnT8 in combination with a specific variant of the zinc transporter gene were associated with an elevated diabetes risk. The researchers claims that "Autoantibodies to ZnT8 are an additional important marker for the progression of diabetes – especially in children who are already developing islet autoantibodies. Hence larger the number of different kinds of autoantibodies, the higher the risk for diabetes, and the younger the child with autoantibodies, the earlier disease onset will be. Its a good achievement. Congrats....

Ref : http://www.helmholtz-muenchen.de/en/press-and-media/press-releases/press-releases-2009/press-releases-2009-detail/article/12322/9/index.html