Velázquez O C, Lederer H M, Rombeau J L
Department Harrison Department of Surgical Research, University of Pennsylvania Medical Center, Philadelphia, USA.
Dig Dis Sci. 1996 Apr;41(4):727-39. doi: 10.1007/BF02213129.
Butyrate is produced in the colon of mammals as a result of microbial fermentation of dietary fiber, undigested starch, and proteins. Butyrate may be an important protective agent in colonic carcinogenesis. Trophic effects on normal colonocytes in vitro and in vivo are induced by butyrate. In contrast, butyrate arrests the growth of neoplastic colonocytes and inhibits the preneoplastic hyperproliferation induced by some tumour promoters in vitro. We speculate that selective effects on G-protein activation may explain this paradox of butyrate's effects in normal versus neoplastic colonocytes. Butyrate induces differentiation of colon cancer cell lines. It also regulates the expression of molecules involved in colonocyte growth and adhesion and inhibits the expression of several protooncogenes relevant to colorectal carcinogenesis. Additional studies are needed to evaluate butyrate's antineoplastic effects in vivo and to understand its mechanism(s) of action.
丁酸盐是哺乳动物结肠中膳食纤维、未消化淀粉和蛋白质经微生物发酵产生的。丁酸盐可能是结肠癌变过程中的一种重要保护剂。丁酸盐在体外和体内均可诱导对正常结肠细胞的营养作用。相反,丁酸盐可抑制肿瘤性结肠细胞的生长,并在体外抑制某些肿瘤启动子诱导的肿瘤前过度增殖。我们推测,对G蛋白激活的选择性作用可能解释了丁酸盐对正常与肿瘤性结肠细胞作用的这一矛盾现象。丁酸盐可诱导结肠癌细胞系分化。它还调节参与结肠细胞生长和黏附的分子表达,并抑制与结直肠癌发生相关的几种原癌基因的表达。需要进一步研究以评估丁酸盐在体内的抗肿瘤作用,并了解其作用机制。