Abstract
Nutritional adversity during development influences the cardiometabolic adaptation in adulthood. Recent birth cohort studies from South Asia have reported an association between maternal folate and vitamin B12 imbalance and increased child adiposity and insulin resistance. In Canada, where folic acid fortification was implemented in 1998, women have adequate folate status but 1 in 20 may be vitamin B12 deficient in the early stages of pregnancy. The goal of our project was to determine the effects of developmental exposure to high folic acid and low vitamin B12 status on vascular function. Female wild‐type C57BL/6J mice were fed diets high in folic acid, with (HFA+B12) and without (HFA‐B12) adequate vitamin B12, or a control diet for six weeks prior to breeding, and during pregnancy and lactation. Offspring were weaned onto control or a western diet (WD), consisting of 45% fat and 35% carbohydrate, and fed for 20 weeks. We assessed vascular endothelial function and NADPH oxidase subunit (Nox2) expression as indicators of vascular health. Mesenteric arteries from WD‐fed mice with developmental exposure to HFA‐B12 showed decreased relaxation (10%) in response to acetylcholine relative to control and HFA+B12 groups. In the control diet group basal nitric oxide production was lower (10%) in mice with developmental exposure to HFA (with and without vitamin B12). Nox2 subunit expression was decreased in aortae of mice with developmental exposure to high folic acid in both control‐fed and WD‐fed mice. These findings suggest that the developmental exposure to high maternal folic acid programs vascular health in adult offspring mice.Grant Funding Source: NSERC
Published Version
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