SCOPE: High glycemic load diets have been associated with increased breast cancer risk in population-based studies, but the evidence is mixed. This investigation determined whether diets differing in glycemic load affected the carcinogenic process using a preclinical model. METHODS AND RESULTS: Human diets, formulated to differ 2-fold in glycemic load, were evaluated in the 1-methyl-nitrosourea-induced (37.5 mg/kg) mammary carcinogenesis model. Cancer incidence (23.3 versus 50.0%, p = 0.032), multiplicity, (0.40 versus 1.03, p = 0.030) and burden, (0.62 versus 1.19 g/rat, p = 0.037) were reduced in the low versus high glycemic load diets, respectively. However, the low glycemic protective effect was attenuated when two purified diets that differed in resistant starch and simulated the glycemic effects of the human diets were fed. Protection was associated with alterations in markers of cell growth regulation. CONCLUSION: Our findings show that human low or high glycemic load dietary patterns differentially affect the carcinogenic response in a nondiabetic rodent model for breast cancer. However, factors that are associated with these patterns, in addition to dietary carbohydrate availability, appear to account for the differences observed.
SCOPE: High glycemic load diets have been associated with increased breast cancer risk in population-based studies, but the evidence is mixed. This investigation determined whether diets differing in glycemic load affected the carcinogenic process using a preclinical model. METHODS AND RESULTS:Human diets, formulated to differ 2-fold in glycemic load, were evaluated in the 1-methyl-nitrosourea-induced (37.5 mg/kg) mammary carcinogenesis model. Cancer incidence (23.3 versus 50.0%, p = 0.032), multiplicity, (0.40 versus 1.03, p = 0.030) and burden, (0.62 versus 1.19 g/rat, p = 0.037) were reduced in the low versus high glycemic load diets, respectively. However, the low glycemic protective effect was attenuated when two purified diets that differed in resistant starch and simulated the glycemic effects of the human diets were fed. Protection was associated with alterations in markers of cell growth regulation. CONCLUSION: Our findings show that human low or high glycemic load dietary patterns differentially affect the carcinogenic response in a nondiabetic rodent model for breast cancer. However, factors that are associated with these patterns, in addition to dietary carbohydrate availability, appear to account for the differences observed.
Authors: S Sieri; V Pala; F Brighenti; C Agnoli; S Grioni; F Berrino; F Scazzina; D Palli; G Masala; P Vineis; C Sacerdote; R Tumino; M C Giurdanella; A Mattiello; S Panico; V Krogh Journal: Nutr Metab Cardiovasc Dis Date: 2012-04-10 Impact factor: 4.222
Authors: Henry J Thompson; Lee W Jones; Lauren G Koch; Steven L Britton; Elizabeth S Neil; John N McGinley Journal: Carcinogenesis Date: 2017-09-01 Impact factor: 4.944