Diabetes & Obesity Drug Discovery & Therapy (Track)




ISOLATION AND STRUCTURAL DETERMINATION OF TWO NOVEL COMPOUNDS FOR THE CONTROL OF DIABETES MELLITUS AND OBESITY

Sayed K. Goda

Anti-Doping Lab-Qatar, Protein Engineering unit, Doha Qatar

Abstract:

Non-insulin-dependent diabetes mellitus (NIDDM), which is one of the main adult diseases, is caused by the secretory decrease in insulin from pancreatic Langerhans cell and/ or peripheral cells become resistant to the action of insulin as in case of obesity. Serious side effects such as retinopathy, neuropathy, and cataracts are also brought about by its long-term manifestation. At present, the direct clinical therapy in NIDDM is to optimize or control the postprandial blood glucose (PBG) level. Polysaccharide degrading enzyme, such as alpha amylase catalyzes the cleavage of starch to produce glucose and other smaller polysaccharides which leads to the increase of the glucose level in the blood. Thus, the retardation of the action of this enzyme by suitable inhibitors may be one of the most effective approaches to control NIDDM. The aim of this work therefore, is to screen for novel inhibitors for human polysaccharide degrading enzymes, salivary and pancreatic alpha-amylases, using natural resources and synthetic compounds. We prepared the total extracts of several herbs and plants collected from different locations in Egypt and in Qatar. Our study demonstrated that the total extract of four plants showed a significant inhibition of the both human alpha-amylase. The active compound from two plants has been isolated and its structure has been determined. 

We also carried out the inhibition study using hundreds of synthetic compounds. The Three synthetic compounds with a significant but variable degree of inhibition of human saliva alpha amylase have been identified.

The novel inhibitors isolated in this study could form the base for clinical trials to demonstrate the effectiveness of these compounds in lowering the glucose level in NIDDM patients and obese people.