Abstract
Maternal nutrition and the intrauterine environment are important in determining susceptibility to reproductive and metabolic disturbances. Advanced glycation end products (AGEs) are widely consumed in Western diet. The purpose of this study was to determine whether perinatal exposure to a high levels of dietary AGEs affect metabolic and reproductive parameters in female mice offspring. Female CD1 mice, 7 weeks old, were placed on either a diet low (L-AGE) or high (H-AGE) in AGEs before mating and then during pregnancy and lactation. All offspring were weaned onto the L-AGE diet and studied through to 16 weeks of age; they were counted and weighed at birth and then every week for a total of 11 weeks. Vaginal opening, litter size, growth curve, liver and abdominal fat weights, serum levels of anti-Mullerian hormone, leptin and adiponectin, as well as insulin and glucose tolerance tests were compared. Ovaries were harvested for follicular count and gene expression by real-time polymerase chain reaction. Compared to perinatal exposure to the L-AGE diet, perinatal exposure to the H-AGE diet caused lower body weight at birth, and adult offspring exhibited delayed growth, lower serum leptin and adiponectin levels, delayed vaginal opening, irregular oestrous cyclicity, arrested follicular development and significant alterations in the expression of genes involved in folliculogenesis (Amh and Amhr2) and steroidogenesis (Cyp19a1). These results indicate that perinatal exposure to a diet elevated in AGEs causes deficits in perinatal growth, pubertal onset, and reproductive organ development in female mice. Whether these findings translate to humans remains to be determined in future studies.
Perinatal exposure to high dietary advanced glycation end products in transgenic NOD8.3 mice leads to pancreatic beta cell dysfunction
