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Anti-amylase, anti-glucosidase and anti-angiotensin I-converting ezyme potential of selected foods

Author:
McCue, P., Kwon, Y.I., Shetty, K.
Source:
Journal of food biochemistry 2005 v.29 no.3 pp. 278-294
ISSN:
0145-8884
Subject:
hyperglycemia, postprandial state, plant-based foods, glycemic effect, alpha-amylase, alpha-glucosidase, angiotensin I, enzyme inhibitors, enzyme inhibition, phenolic compounds, traditional foods, phytochemicals, antioxidant activity, United States, Asia
Abstract:
alpha-Amylase and alpha-glucosidase have been targeted as potential avenues for modulation of postprandial hyperglycemia through mild inhibition of the enzymatic breakdown of complex carbohydrates to decrease meal-derived glucose absorption. Water-soluble extracts with optimized phenolic content of selected American and Asian foods were investigated for inhibitory activity against alpha-amylase and alpha-glucosidase, as well as angiotensin I-converting enzyme (ACE), which has been linked to hyperglycemia-associated hypertension. Porcine pancreatic alpha-amylase (PPA) was allowed to react with each phenolic-optimized food extract, and the derivatized enzymephytochemical mixtures obtained were characterized for residual amylase activity. The alpha-glucosidase and ACE activities were determined in the presence of each phenolic-optimized food extract. The amylase activity was inhibited more than the glucosidase activity in the presence of these phytochemical extracts, and more so by Asian foods than by American foods. The Asian spice ginger was found to possess strong ACE inhibitory activity in addition to significant anti-amylase activity. The alpha-amylase enzyme inhibition was positively associated with extract antioxidant activity and negatively with extract protein content. The significance of food-grade, plant-based amylase inhibitors for modulation of carbohydrate breakdown and control of glycemic index of foods in the context of preventing hyperglycemia and diabetes mellitus complications in the long term and ACE inhibitors for modulation of associated hypertension is hypothesized and discussed.
Agid:
1413385