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果胶通过肠道菌群介导宿主血糖调节的机制。

Pectin mediates the mechanism of host blood glucose regulation through intestinal flora.

机构信息

College of Food Science, Sichuan Agricultural University, Ya'an, China.

出版信息

Crit Rev Food Sci Nutr. 2024;64(19):6714-6736. doi: 10.1080/10408398.2023.2173719. Epub 2023 Feb 9.

DOI:10.1080/10408398.2023.2173719
PMID:36756885
Abstract

Pectin is a complex polysaccharide found in plant cell walls and interlayers. As a food component, pectin is benefit for regulating intestinal flora. Metabolites of intestinal flora, including short-chain fatty acids (SCFAs), bile acids (BAs) and lipopolysaccharides (LPS), are involved in blood glucose regulation. SCFAs promote insulin synthesis through the intestine-GPCRs-derived pathway and hepatic adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) pathway to promote hepatic glycogen synthesis. On the one hand, BAs stimulate intestinal L cells and pancreatic α cells to secrete Glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) through receptors G protein-coupled receptor (TGR5) and farnesoid X receptor (FXR). On the other hand, BAs promote hepatic glycogen synthesis through AMPK pathway. LPS inhibits the release of inflammatory cytokines through Toll-like receptors (TLRs)-myeloid differentiation factor 88 (MYD88) pathway and mitogen-activated protein kinase (MAPK) pathway, thereby alleviating insulin resistance (IR). In brief, both SCFAs and BAs promote GLP-1 secretion through different pathways, employing strategies of increasing glucose consumption and decreasing glucose production to maintain normal glucose levels. Notably, pectin can also directly inhibit the release of inflammatory cytokines through the -TLRs-MYD88 pathway. These data provide valuable information for further elucidating the relationship between pectin-intestinal flora-glucose metabolism.

摘要

果胶是一种存在于植物细胞壁和中层的复杂多糖。作为一种食物成分,果胶有益于调节肠道菌群。肠道菌群的代谢物,包括短链脂肪酸(SCFAs)、胆汁酸(BAs)和脂多糖(LPS),参与血糖调节。SCFAs 通过肠-GPCR 衍生途径和肝腺苷 5'-单磷酸(AMP)激活蛋白激酶(AMPK)途径促进胰岛素合成,从而促进肝糖原合成。一方面,BAs 通过 G 蛋白偶联受体(TGR5)和法尼醇 X 受体(FXR)刺激肠 L 细胞和胰腺α细胞分泌胰高血糖素样肽-1(GLP-1)和肽 YY(PYY)。另一方面,BAs 通过 AMPK 途径促进肝糖原合成。LPS 通过 Toll 样受体(TLRs)-髓样分化因子 88(MYD88)途径和丝裂原活化蛋白激酶(MAPK)途径抑制炎症细胞因子的释放,从而减轻胰岛素抵抗(IR)。简而言之,SCFAs 和 BAs 通过不同途径促进 GLP-1 的分泌,采用增加葡萄糖消耗和减少葡萄糖产生的策略来维持正常的血糖水平。值得注意的是,果胶还可以通过-TLRs-MYD88 途径直接抑制炎症细胞因子的释放。这些数据为进一步阐明果胶-肠道菌群-葡萄糖代谢之间的关系提供了有价值的信息。

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