Harris P J, Ferguson L R
School of Biological Sciences, University of Auckland, New Zealand.
Mutat Res. 1993 Nov;290(1):97-110. doi: 10.1016/0027-5107(93)90037-g.
Dietary fibre has a complex and highly variable composition. Although some dietary fibres may protect against colorectal cancer, it is unlikely that all are equally protective. Dietary fibre is principally composed of plant cell walls, but it also includes components obtained from cell walls (e.g. cellulose, pectin, and lignin), and non-starch polysaccharides (NSPs) from other sources (e.g. seaweeds and micro-organisms). The AOAC and Englyst methods are commonly used to determine the total amount of dietary fibre in foods. Most of the cell walls in food plants are from parenchyma cells, which are extensively degraded by bacteria in the colon. Cell types with walls containing the hydrophobic polymers lignin, suberin, or cutin also occur in food plants in small numbers, but they may be important in preventing colorectal cancer. Lignin, and possibly the other polymers, protect these walls from degradation. Epidemiological, human intervention, and animal studies can be used to try to identify the most protective dietary fibres. Epidemiological studies are difficult to interpret because usually only the total amount of dietary fibre eaten is reported. Intervention studies indicate that wheat bran dietary fibre may be protective. The results of animal carcinogenesis studies are variable, but sources of insoluble dietary fibres, including wheat bran, appear more protective than soluble dietary fibres, and some dietary fibres appear to enhance carcinogenesis. Possible mechanisms for protection by dietary fibres can be divided into two groups: those where the dietary fibre is acting directly, and those which result from the dietary fibre being degraded by colonic bacterial enzymes and the products fermented. Possible direct mechanisms include the binding of carcinogens to undegradable dietary fibres, and the absorption of water by undegradable dietary fibre resulting in increased faecal bulk and shortened transit times. Possible indirect mechanisms include the lowering of the colon pH by the short-chain fatty acids produced by bacterial fermentation, and the specific effects of butyrate. There are also a number of possible mechanisms by which some dietary fibres may enhance carcinogenesis. Use of better defined dietary fibres will increase our understanding of the role of dietary fibres in modulating colorectal cancer.
膳食纤维具有复杂且高度可变的组成。尽管某些膳食纤维可能预防结直肠癌,但不太可能所有膳食纤维都具有同等的保护作用。膳食纤维主要由植物细胞壁组成,但它还包括从细胞壁获得的成分(如纤维素、果胶和木质素),以及来自其他来源(如海藻和微生物)的非淀粉多糖(NSPs)。AOAC法和恩格里斯法常用于测定食品中膳食纤维的总量。食用植物中的大多数细胞壁来自薄壁细胞,这些细胞壁在结肠中会被细菌大量降解。食品植物中也少量存在含有疏水性聚合物木质素、木栓质或角质的细胞壁类型的细胞,但它们在预防结直肠癌方面可能很重要。木质素以及其他可能的聚合物可保护这些细胞壁不被降解。流行病学、人体干预和动物研究可用于试图确定最具保护作用的膳食纤维。流行病学研究难以解释,因为通常只报告膳食纤维的总摄入量。干预研究表明,麦麸膳食纤维可能具有保护作用。动物致癌研究的结果各不相同,但包括麦麸在内的不溶性膳食纤维来源似乎比可溶性膳食纤维更具保护作用,而且某些膳食纤维似乎会促进致癌作用。膳食纤维发挥保护作用的可能机制可分为两类:一类是膳食纤维直接起作用,另一类是膳食纤维被结肠细菌酶降解并发酵产物所产生的机制。可能的直接机制包括致癌物与不可降解的膳食纤维结合,以及不可降解的膳食纤维吸收水分导致粪便量增加和运输时间缩短。可能的间接机制包括细菌发酵产生的短链脂肪酸降低结肠pH值,以及丁酸的特定作用。也有一些膳食纤维可能促进致癌作用的可能机制。使用定义更明确的膳食纤维将增进我们对膳食纤维在调节结直肠癌中作用的理解。