食品科学 ›› 2022, Vol. 43 ›› Issue (5): 264-274.doi: 10.7506/spkx1002-6630-20210223-258

• 专题论述 • 上一篇    下一篇

“抗性淀粉-肠道菌群-代谢产物”营养轴的研究进展

何书琪,童铭瑶,雷素珍,张怡,曾红亮   

  1. (1.福建农林大学食品科学学院,福建 福州 350002;2.福建省特种淀粉品质科学与加工技术重点实验室,福建 福州 350002;3.中爱国际合作食品物质学与结构设计研究中心,福建 福州 350002)
  • 发布日期:2022-03-28
  • 基金资助:
    国家自然科学基金面上项目(31972076);福建省自然科学基金杰出青年项目(2019J06012); 福建省科技经济融合服务平台资助项目

Advances in Research on the “Resistant Starch-Intestinal Flora-Metabolite” Nutrition Axis

HE Shuqi, TONG Mingyao, LEI Suzhen, ZHANG Yi, ZENG Hongliang   

  1. (1. College of Food Science, Fujian Agriculture and Forestry University, Fuzhou 350002, China; 2. Fujian Provincial Key Laboratory of Quality Science and Processing Technology in Special Starch, Fuzhou 350002, China; 3. China-Ireland International Cooperation Centre for Food Material Science and Structure Design, Fuzhou 350002, China)
  • Published:2022-03-28

摘要: 抗性淀粉(resistant starch,RS)在小肠内不易消化吸收,但可被大肠肠道菌群利用产生短链脂肪酸等代谢物并调节肠道菌群平衡,促进短链脂肪酸的产生及调节胆汁酸代谢。因此,本文构建“RS-肠道菌群-代谢产物”营养轴系统,概述RS调控肠道菌群介导代谢物产生的作用机制,比较菌群发酵对RS表观结构、晶体结构和分子结构产生的影响,阐述RS结构特性与肠道菌群群落结构、短链脂肪酸产量和胆汁酸排泄之间的关系,总结RS通过调节肠道菌群及肠道代谢物改善代谢性疾病的作用机制。此外,进一步展望RS-肠道菌群-胆汁酸之间的作用途径以及RS在代谢性疾病中与胆汁酸和短链脂肪酸的作用机制。

关键词: 抗性淀粉;肠道菌群;代谢产物;结构特性;短链脂肪酸;胆汁酸

Abstract: Resistant starch is not easily digested and absorbed in the small intestine, but it can be utilized by the large intestinal microflora to produce metabolites such as short-chain fatty acids, which in turn can regulate the intestinal microfloral balance and bile acid metabolism. Therefore, this article puts forward the “resistant starch-intestinal flora-metabolite” nutrition axis to systematically summarize the mechanism of action by which RS mediates the production of metabolites by regulating the intestinal microflora. It compares the effects of intestinal microbial fermentation on the apparent, crystal and molecular structure of RS, describes the relationship of the structural characteristics of RS with the intestinal community structure, the production of short-chain fatty acids and the excretion of bile acids, and summarizes the mechanism of RS for improving metabolic diseases by regulating the intestinal microflora and intestinal metabolites. Besides, an outlook is given on future studies on the pathways of the interaction among resistant starch, the intestinal microflora and bile acid, and on the mechanism of RS interaction with bile acids and short-chain fatty acids in metabolic diseases.

Key words: resistant starch; intestinal microflora; metabolites; structural properties; short chain fatty acids; bile acids

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