## 3 Results and Discussion
### Pharmacological Activities  
#### 3.3.1 Oral Glucose Tolerance Test (OGTT)  
The impact of the two extracts from _S. eleagenifolium_ on normal rats subjected to oral glucose loading is depicted in Figure 3. Prior to administering their respective treatments, there were no notable variations in fasting blood glucose levels across the groups. The outcomes of an oral glucose tolerance test conducted on healthy rats demonstrate that the administration of 2 g/kg of glucose resulted in a baseline blood sugar level of 0.92 g/L for rats in the control group, which received only distilled water. The levels of postprandial hyperglycemia reached a peak at 1.76 \(\pm\) 0.03 g/L after 60 min, and subsequently decreased to an average of 1.02 \(\pm\) 0.08 g/L after 120 min. While a substance known as SEFE was administered at a dose of 150 mg/kg, it significantly suppressed postprandial hyperglycemia in comparison to the control group's rats. This suppression was observed at multiple time points: after 30 min (_p_ < 0.01) with a reading of 0.98 \(\pm\) 0.02 g/L, after 60 min (_p_ < 0.001) with a reading of 1.04 \(\pm\) 0.03 g/L, and at 120 min (_p_ < 0.01) with a reading of 0.85 \(\pm\) 0.01 g/L. 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 60 min (_p_ < 0.001) with a reading of 1.03 \(\pm\) 0.009 g/L, and at 120 min (_p_ < 0.01) with a reading of 0.86 \(\pm\) 0.01 g/L. The outcomes of an oral glucose tolerance test conducted on healthy rats demonstrate that the administration of 2 g/kg of glucose resulted in a baseline blood sugar level of 0.92 g/L for rats in the control group, which received only distilled water. The levels of postprandial hyperglycemia reached a peak at 1.76 \(\pm\) 0.03 g/L after 60 min, and subsequently decreased to an average of 1.02 \(\pm\) 0.08 g/L after 120 min. While a substance known as SEFR was administered at a dose of 150 mg/kg, it significantly suppressed postprandial hyperglycemia in comparison to the control group's rats. This suppression was observed after 30 min (_p_ < 0.001) with a reading of 1.15 \(\pm\) 0.04 g/L. In contrast, when SEFR 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_ < 0.05) with a reading of 0.94 \(\pm\) 0.02 g/L, at 60 min (_p_ < 0.001) with a reading of 0.83 \(\pm\) 0.06 g/L, and at 120 min (_p_ < 0.01) with 0.79 \(\pm\) 0.03 g/L. The SEFR extract at a dose of 300 mg/kg appears to exhibit the most significant antihyperglycemic potential among the tested extracts and glibenclamide. This is evident from its more pronounced suppression of postprandial hyperglycemia at multiple time points and lower blood glucose levels compared to the other tested extracts and doses. Oral glucose loading causes diabetes mellitus by gradually raising blood glucose levels without harming pancreatic cells. As a result, whether an ex  
Figure 2: (**A**) Anti-lipase effect of SEFR, SEFE, and Orlistat; and (**B**) inhibitory effect of SEFR, SEFE, and gallic acid (positive control) on glycation activity of hemoglobin. Results are shown as mean \(\pm\) SEM (n = 3). tract reduced blood glucose levels in rats after an oral glucose load indicates its therapeutic potential in diabetes management [37]. 3.2 Inhibition of Carbohydrate Hydrolase Enzymes, In Vivo In Vivo Anti-\(\alpha\)-Amylase Activity of _S. elaagenifolium_ Leaves and Fruits  
In the pursuit of treating diabetes mellitus, one of the targeted pathways involves inhibiting sugar-digesting enzymes, specifically pancreatic \(\alpha\)-amylase.