The blood glucose level is controlled as a feature of metabolic homeostasis (Young, 1977). The ordinary scope of glucose in the plasma is managed between 3.5-8.0 mM (Arciero et al., 1999). The degree of the sugar in the blood outside the ordinary range might be characteristic of an ailment. A constantly elevated level in blood glucose is alluded to as hyperglycemia and low glucose levels are alluded to as hypoglycemia (Colberg and Colberg, 2009; Lee et al., 2005). Glucose shipped from the digestion tracts or liver to the body cells is made accessible for take-up by assimilation cells and digestion (Reddy, 2012). The islets of Langerhans in the pancreas arranges the discharge of insulin and glucagon (Lowell and Shulman, 2005; Quesada et al., 2008). If the blood glucose levels rise the ß-cells import and oxidize glucose to help mitochondrial ATP blend. This procedure animate an ascent in the cytoplasmic ATP/ADP proportion, which thusly instigates the Ca2+ take-up from mitochondria pursued by an arrival of insulin (Maechler et al., 2010; MacDonald et al., 2005). After its discharge the insulin guarantees the take-up of glucose from delicate tissues, digestion and capacity of glucose as glycogen or lipids. Insulin can neutralize the impacts of glucagon in the liver. This happens by restraint of gluconeogenesis and glycogenolysis. Low blood glucose levels brief the discharge of glucagon which thus instigates glyconeogenesis and glucose assembly in the hepatic tissue. These procedures at that point reestablishes euglycemia and at the principle time counteract insulin activity (Quesada et al., 2008). If there is an interruption in the planned discharge of insulin and glucagon, it might prompt enduring obsessive impacts, including the improvement of type1 diabetes (T1DM) and type2 diabetes (T2DM). Both T1DM and T2DM are portrayed by continuous disappointment and devastation of the ß-cells. T2DM creates through an unpredictable transaction among hereditary qualities and natural factors, for example, presentation to poisons, diet and liquor utilization (Cnop et al., 2005). T1DM is portrayed by an auto-safe ambush, which happens with the intrusion of the islets by mononuclear cells and enlistment of intra-islet irritation and cell apoptosis (Knip et al., 2005). Improvement of T1DM can likewise be encouraged by presentation to synthetic concoctions. Synthetic substances, for example, alloxan and streptozotocin are frequently regulated to specifically annihilate ß cells and incite T1DM. The two compound substances kill ß cells by instigating oxidative pressure and harm by disturbing pancreatic particle transport and calcium levels (Szkudelski, 2001). The significant wellspring of blood glucose is dietary sugars, for example, starch, which are hydrolyzed by a-glucosidases and pancreatic a-amylase, in order to be consumed by the small digestive tract. Inhibitors of the proteins could hinder the take-up of dietary starches, which stifle postprandial hyp