AI Article Synopsis
- - The rapid digestion of starch in our diet causes spikes in blood sugar, and inhibiting α-amylase can help control these spikes by reducing starch digestibility.
- - Microbial exopolysaccharides (EPSs), especially those produced by lactic acid bacteria, show promise in inhibiting α-amylase, thereby potentially lowering blood glucose levels and improving glycolipid metabolism.
- - This review discusses the mechanisms of how microbial EPSs work and suggests their potential use in functional foods and pharmaceuticals to help manage blood sugar and support gut health.
Article Abstract
The rapid digestion of starch, as the main source of energy in the human diet, causes an acute increase in blood sugar levels that will affect blood glucose homeostasis. The inhibition of α-amylase activity is an effective way of reducing starch digestibility, thereby controlling postprandial glycemia. As a class of carbohydrate polymers, microbial exopolysaccharides (EPSs) have garnered widespread attention for their inhibitory effects on α-amylase, but there is a lack of comprehensive review in this area. This paper aimed to review the inhibitory activity of microbial EPSs on α-amylase and their interaction mechanisms, and the effect of microbial EPSs on lowering blood glucose levels and regulating glycolipid metabolism in vivo were also discussed. Numerous studies have reported that EPSs with α-amylase inhibition activity are primarily produced by lactic acid bacteria. Microbial EPSs with an appropriate range of molecular weight, high proportion of glucose or mannose or arabinose residues, and high uronic acid content might be acceptable to inhibit α-amylase activity. Additionally, microbial EPSs exhibited potential anti-diabetic effects in mice, reducing blood glucose levels, and regulating glycolipid metabolism and gut microbiota. The information covered in this review may enhance the development and application of EPSs in functional food and pharmaceutical research.
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| http://dx.doi.org/10.1016/j.ijbiomac.2024.136174 | DOI Listing |
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