Modulation of paternal B vitamin intake does not affect tumorigenesis but does alter growth trajectory in Apc^1638N mouse offspring (137.7)

Abstract

Modulation of paternal B vitamin intake does not affect tumorigenesis but does alter growth trajectory in Apc1638N mouse offspring Sabet JA1,2, Mason JB1,2, Bronson RT3, Crott JW1,21Friedman School of Nutrition Science and Policy at Tufts University, Boston, MA2Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA3Rodent Histopathology Core, Harvard Medical School, Boston, MA It is well established that maternal nutrition can impact on offspring health and physiology; however the contribution of paternal nutrition to offspring health is less understood. We have shown that maternal B‐vitamin supplementation suppresses, while deficiency promotes, intestinal tumorigenesis in a mouse model of colorectal cancer. We sought to determine whether modulating paternal intake of vitamins B2, B6, B12, and folate similarly alters intestinal tumorigenesis in offspring. Male APC1638N mice were fed diets containing control, deficient, or supplemental quantities of vitamins B2, B6, B12, and folate for 8 wk before mating with control‐fed wild‐type females. APC1638N offspring were maintained on control diets until 28 wk of age. No differences in tumor incidence, size or grade were found between offspring of different paternal diet groups. Overall, male offspring exhibited a greater tumor incidence and burden than female offspring. Among female offspring, growth was significantly retarded in the progeny of deficient and supplemented fathers compared to control fathers. Modulation of paternal B‐vitamin intake prior to mating did not alter offspring intestinal tumorigenesis but did impact offspring growth in a sex‐specific fashion in APC1638N mice. Analyses to profile DNA methylation changes in sperm and gene expression changes in offspring liver are underway. Grant Funding Source: Supported by NCI grant 1 R03CA162505‐1