## 4 Discussion
### Antidiabetic Activity  
Two carbohydrate-hydrolyzing enzymes (\(\alpha\)-amylase and \(\alpha\)-glucosidase) are primarily responsible for postprandial hyperglycemia. \(\alpha\)-Amylase initiates carbohydrate digestion by hydrolyzing polysaccharide (1,4-glycosidic linkages) into disaccharides. Postprandial hyperglycemia is caused by \(\alpha\)-glucosidase, which catalyzes the conversion of disaccharides to monosaccharides [34]. As a result, \(\alpha\)-amylase and \(\alpha\)-glucosidase inhibitors assist in hyperglycemia management by slowing carbohydrate digestion, thus reducing postprandial plasma glucose levels [35; 36]. Insulin promotes glucose reduction by increasing the transfer of glucose from the circulation into skeletal muscle cells. Insulin-stimulated glucose uptake is well known to be diminished in individuals with type II diabetes [37]. Therefore, identifying compounds that might increase glucose absorption is an essential first step in the development of novel strategies for treating insulin resistance [38]. As reported above, the gas chromatographic analysis highlighted the predominance of fatty acids, sesquiterpenes, and monoterenes. Linolenic acid and myrisic acid were the predominant fatty acids. p-Cymene and spathulenol predominate among the monoterenes and sesquiterpenes, respectively. Fatty acids can contribute to the regulation of metabolic syndrome by acting on lipid and glucose metabolism, as previously reported [39; 40; 41]. For example, chronic administration of myrisic acid reduces insulin resistance and body weight in animal models [42]. Linolenic acid can also contribute to the regulation of glucose metabolism, as recently reported [43]. Amylases and glucosidases can also interact with terpenoids. [PERSON] et al. observed that treatment with terpenoids can improve insulin resistance by acting on amylase and glucosidase [44]. As with the extracts of many plant species, the entourage effect of other components cannot be excluded [45]. Indeed, when evaluating the therapeutic effect of a plant extract, it is necessary to consider the entire phytocomplex [46]. Therefore, the other components present in _C. incana_ can influence carbohydrate metabolism. Furthermore, type II diabetes can be induced by insulin-producing pancreatic cell malfunction, which can be initiated by an excessive lipid build-up in the pancreas [47]. Pancreatic lipase is the primary enzyme responsible for dietary fat absorption in the gastrointestinal system via breakdown of triacylglyceredyns (TGs) into free fatty acids (FFAs) and monoacylglycerolcords (MAGs) [48]. Recently, researchers have been interested in pancreatic lipase inhibitors because of their anti-obesity effects, which act by delaying lipolytic processes. This action minimizes fat absorption, protects the pancreas, and restores normal cellular insulin generation [48]. Terpenoids may have an anti-obesity effect by acting as inhibitors of pancreatic lipase, as previously reported [49]. Furthermore, linolenic and myrisic acids have lipase-mediated anti-obesity action. Dipeptidyl peptidase IV (DPP-IV) is a ubiquitous enzyme involved in the rapid metabolism of incrin hormones, primarily glucagon-like peptide-1(GLP-1) and gastric inhibitory peptide (GIP), which maintain glucose homeostasis by increasing insulin secretion and reducing glucagon secretion [50]. Thus, DPP-IV inhibitors can prolong the action of cretrins. Since increasing stimulate glucose-dependent insulin secretion from the pancreas, inhibiting DPP-IV is a unique therapeutic strategy for treating type II diabetes [18; 51; 52; 53; 54; 55]. Therefore, the results of this study showed that the ethanolic extract of _C. incana_ inhibited \(\alpha\)-amylase, \(\alpha\)-glucosidase, and pancreatic lipase, but not DPP-IV, compared with the respective positive controls. This indicates that the ethanolic extract of _C. incana_ possesses an antidiabetic mechanism involving the inhibition of these enzymes.