Non-digestible carbohydrates reduce growth of estrogen-dependent breast cancer in mice
A new study has reported that consuming non-digestible carbohydrates may have a protective effect against estrogen receptor positive (ER+) tumors by inhibiting cellular proliferation and increasing apoptosis. Non-digestible carbohydrates cannot be broken down in the gastrointestinal tract by acids and digestive enzymes before reaching the colon (where they are fermented). Some non-digestible carbohydrates are used as prebiotics since they can selectively promote the growth of certain intestinal bacteria that support healthy colon conditions. Non-digestible carbohydrates such as maltodextrin have also been used as low-calorie sweeteners.
The study was designed to investigate the dietary effect of commercially available non-digestible carbohydrates on hormone receptor positive (MCF-7) human breast cancer tumors implanted in mice with their ovaries removed (simulating the postmenopausal state). The mice were administered the estrogen 17β-estradiol (E2) to promote tumor growth. The animals were then divided into groups and fed diets including 5% non-digestible carbohydrate (fructooligosaccharides, Fibersol 2 (digestion resistant maltodextrin), Hi-Maize (high amylose cornstarch), or Frutafit (a range of powdered inulins)) or a control diet without non-digestible carbohydrates. Inulin is a non-digestible soluble fiber found in cereal grains, onions, garlic and many other commonly consumed plants.
Mice fed diets containing Fibersol 2, Hi-Maize, or fructooligosaccharides were found to have significantly reduced tumor growth compared to the control mice. Cellular proliferation was inhibited and apoptosis (a type of cell death initiated to rid the body of defective and other unwanted cells) was increased in the tumors of these mice. Mice fed Fibersol 2, Hi-Maize, or fructooligosaccharides also had lower circulating estradiol levels and reduced uterine weight compared to mice on the control diet. In addition, non-digestible carbohydrates were shown to reduce expression of the estradiol-responsive gene markers in the MCF-7 tumors.