The effect may be due to stimulation of insulin release by pancreas or due to delayed glucose absorption.[15] Delayed glucose absorption is usually due to inhibition of enzyme α-glucosidase located at intestinal surface.[16] Liver plays an important role in buffering the postprandial hyperglycemia and is involved in the synthesis of glycogen.[2, 17] In NIDDM, normal capacity of liver to synthesize glycogen is impaired. This evidence concerns the gene INS and Hyperglycemia.