The inhibitory effect of dietary fructose on lactation‐induced increases in rat epithelial calcium transport is mediated by fructose‐induced reductions in vitamin D levels

Abstract

Pregnancy and lactation require marked increases in consumption and transport of dietary Ca2+ to maintain Ca2+ homeostasis and bone health. This increase in epithelial Ca2+ transport is regulated by increasing levels of calcitriol whose genomic effects are mediated by the vitamin D receptor (VDR). We recently showed that fructose (F) consumption reduced intestinal Ca2+ transport. We used lactating rats as animal model to test whether the deleterious effects of excessive F intake on Ca2+ transport is regulated by calcitriol and lead to bone defects. Pregnant and virgin (control) rats were fed isocaloric 63% F or, as controls, glucose and starch diets from d 2 of gestation to end of lactation. Compared to virgins, lactating dams fed glucose or starch had higher rates of intestinal Ca2+ transport, elevated intestinal and renal expression of Ca2+ transporters, as well as increased levels of calcitriol and 1‐alpha‐hydroxylase. F consumption prevented these lactation‐induced increases, and reduced VDR binding to promoter regions of TRPV6 and CaBP9k. Bone mineral density, content and mechanical strength each decreased with lactation, and this decrease was exacerbated by F diet. In lactating rats with enhanced Ca2+ needs, excessive F intake prevents, through a calcitriol‐dependent pathway, adaptive increases in epithelial Ca2+ transport, likely compromising bone quality (NSF IOS‐1121049, Benjamin Delessert)