Effect of PA extract on enzyme inhibitory effect
Supplementary table 4 explains the effect of the PA extract on the different enzymes. PA showed the IC50 56.4 μg/mL against α-amylase, IC50 220.5 μg/mL against α- glucosidase and IC50 162.9 μg/mL against DPPIV, respectively.
DPP-IV is a member of peptidase family, with 766 amino acids and is distributed in various tissues. It is considered as the hydrolase enzyme and is also present in the circulating. DPP-IV showed their biological effect via two mechanisms, first, by its binding to adenosine deaminase and conveys the independent signal to its enzymatic function via alteration of intracellular singling pathway (Wang et al., 2013). Secondly, its catalytic activity is exhibited by spanning membrane form of a molecule. Various researchers suggest that the DPP-IV mediated inactivation of GLP-1 is the key mediator for the GIP activity that can be targeted by inhibition of DPP-IV as the novel approach for the treatment of DM (Gupta et al., 2009). The inhibition of DPP-IV prevents the degradation of GLP-1 and alters the clearance of GLP-1 from the renal tissue. Normally, GLP-1 takes part in the promotion of insulin secretion from the β-cells, down-regulation of glucogen secretion, enhancing masses of β-cells, inducing satiety and diminution of gastric emptying rate, which helps to maintain the normal level of BGL in type II diabetes mellitus (Seino et al., 2010; Meier, 2012).
α-amylase cleavage the glycosidic bond. Glycoside with glycosidic bond linkage can change the role of starch substrate. According to this mechanism, starch is not converted into disaccharide in the body and help to promote the action of glucosidase, which converts the disaccharide into monosaccharides and maintain the glucose level in the body (Perić-Hassler et al., 2010).
3.2 Effect of PAextract on oral glucose tolerance test (OGTT)
Figure 1 depicts the effect of the PA extract and glucose control group rats. The figure 1 shows that the normal andPA (200 mg/kg) group rats showed almost similar BGL at end of the experimental study. Glucose control group rats showed the upregulation of BGL after the glucose administration and it reached maximum level (130 mg/Dl) after 30 min. After that, the BGL slightly decreased at end of the experimental study and came to 111 mg/dL. PA received group rats showed the reduction of BGL 100.66 and 96.33 and 81 mg/dL at a dose of 50, 100 and 200 mg/kg, respectively. On the other hand, standard drug (glibenclamide) showed the reduction in the BGL at 73.66 mg/dL.
Figure 1b demonstrates the effect of the PA administration on the OGTT. After glucose load, we observe that the NC and NC receivedPA (200 mg/kg) showed the almost similar AUCglucose value. On the other hand, glucose control group showed the increase AUCglucose as a compared to other groups of rats. PA treatment showed the diminution of AUCglucose at end of the OGTT study. The same results were observed in the glibenclamide treated group rats.
Oral glucose tolerance test (OGTT) was performed for the recognizing the modulation of carbohydrate metabolism during the post glucose treatment (Ahmed et al., 2013, 2014c; Kumar et al., 2014). Glucose control group rats showed the increased BGL at end of the experimental study and glucose control group rats showed the reduction in the BGL after treatment with the PA at dose-dependently. PA showed the marked reduction 7.69%, 29.49% and 37.69% in the BGL at dose 50, 100 and 200 mg/kg, respectively. On the other hand, glibenclamide showed the marked 41.28% reduction in BGL. The result clearly indicates the significant reduction in the BGL and suggests the better utilization capacity. PA showed the decreased BGL may be due to insulin secretion from β-cells and improved the utilization of via glucose consumption.