## 3 Results and Discussion
### Pharmacological Activities
#### 3.3.1 Oral Glucose Tolerance Test (OGTT)
This enzyme plays a crucial role in the initial digestion of disaccharides, which undergo a transformation process comprising both intraluminal and straightforward mechanisms, ultimately resulting in the formation of naturally occurring oligosaccharides [38]. After studying the anti-\(\alpha\)-amylase activity of _S. elaagenifolium_ extracts in vitro, and to confirm the inhibitory activity of _S. elaagenifolium_ SEFE and SEFR extracts on the pancreatic \(\alpha\)-amylase enzyme, the test was performed in vivo using the protocol defined by [PERSON] et al. [39], and the results are shown in Figure 4. After administering 2 g/kg of starch, there was a notable increase in blood glucose levels, peaking at 1.49 \(\pm\) 0.02 g/L. This peak gradually subsided to 1.32 \(\pm\) 0.07 g/L at the 60 min mark. However, upon the administration of SEFE at a dose of 150 mg/kg, a substantial reduction in postprandial blood glucose levels was observed. The reduction was statistically significant at both 30 min (\(p<0.001\)) and 60 min (\(p<0.001\)), with recorded values of 0.9 \(\pm\) 0.01 g/L and 0.83 \(\pm\) 0.002 g/L, respectively, in comparison to the control group. Interestingly, there was no significant difference in blood glucose levels at the 120 min mark. In contrast, when SEFE was administered at a higher dose of 300 mg/kg, it also significantly suppressed postprandial hyperglycemia in comparison to the control group's rats. This suppression was observed at multiple time points: after 30 min (\(p<0.001\)) with a reading of 0.9 \(\pm\) 0.04 g/L, and at 60 min (\(p<0.011\)) with a reading of 0.88 \(\pm\) 0.007 g/L. After administering 2 g/kg of starch, there was a notable increase in blood glucose levels, peaking at 1.49 \(\pm\) 0.02 g/L. This peak gradually subsided to 1.32 \(\pm\) 0.07 g/L at the 60 min mark. However, upon the administration of SEFR at a dose of 150 mg/kg, a substantial reduction in postprandial blood glucose levels was observed. The reduction was statistically significant at 30 min (\(p<0.001\)), 60 min (\(p<0.001\)), and 120 min (\(p<0.01\)), with recorded values of 0.92 \(\pm\) 0.02 g/L, 0.78 \(\pm\) 0.02 g/L, and 0.7 \(\pm\) 0.03 g/L respectively, in comparison to the control group. Interestingly, there was no significant difference in blood glucose levels at the 120 min mark. In contrast, when SEFE was administered at a higher dose of 300 mg/kg, it also significantly suppressed postprandial hyperglycemia in comparison to the control group's rats. This suppression was observed at multiple time points: after 30 min (\(p<0.001\)) with a reading of 0.82 \(\pm\) 0.009 g/L, at 60 min (\(p<0.001\)) with a reading of 0.69 \(\pm\) 0.03 g/L, and at 120 min (\(p<0.001\)) with 0.76 \(\pm\) 0.01 g/L. Furthermore, the introduction of 10 mg/kg of acarbose significantly hindered starch-induced hyperglycemia. The inhibition was significant at both 30 min (\(p<0.001\)) and 60 min (\(p<0.001\)),  
Figure 3: (**A**) Effect of SEFE on rats orally loaded with glucose; and (**B**) effect of SEFR on rats orally loaded with glucose. * \(p<0.05\);** \(p<0.01\); *** \(p<0.001\) as compared to the control. and also showed significance at 120 min (\(p\) < 0.05). The measured blood glucose values were 1.11 \(\pm\) 0.06 g/L, 0.95 \(\pm\) 0.004 g/L, and 0.91 \(\pm\) 0.03 g/L for the respective time points, compared to the control group. The SEFR extract, at a dose of 300 mg/kg, consistently demonstrated the most significant and consistent antihyperglycemic activity across multiple time points, demonstrating that it has the highest antihyperglycemic potency of the tested extracts. Limiting the activity of carbohydrate digestive enzymes in the intestine is one strategy used to reduce postprandial hyperglycemia [40]. \(\alpha\)-amylase inhibitors prevent carbohydrate digestion and absorption in the intestine, resulting in hypoglycemia [41]. In Vivo Anti-\(\alpha\)-Glycosidase Activity of _S.