Marginal iodine deficiency is a major health problem in pregnant women, but its impact on nerve and intelligence development in offspring has been rarely reported. Our study aimed to investigate the effects of maternal marginal iodine deficiency on nerve and cognitive development in offspring and the related mechanisms. Marginal iodine-deficient rats were given 3 μg iodine per day, while normal control rats were given 4 μg iodine daily. Western blot was used to detect the amounts of brain-derived neurotropic factor (BDNF) and early growth response protein 1 (EGR1) in the hippocampus of each group. Immunohistochemistry was used to measure c-jun and c-fos expression in the hippocampal CA1 region. Finally, the water maze method was used to measure spatial performance. Free thyroxine (FT4) levels in marginal iodine-deficient rats decreased by about 30%. Seven days after birth, EGR1 and BDNF protein levels significantly decreased in the hippocampus of marginal iodine deficiency rats compared with the normal control group. In addition, c-jun and c-fos expression in the hippocampus of 40-day-old rats was decreased in marginal iodine-deficient rats, compared with control. The spatial learning and memory ability of 40-day-old marginal iodine-deficient rats had a downward trend compared with the normal control group. FT4 significantly decreased after pregnancy in rats with marginal iodine deficiency, affecting the expression of related proteins in the brain of offspring.
Yuhui Liu, Le Zhang, Jing Li, Zhongyan Shan and Weiping Teng
Caiping Mao, Rong Liu, Le Bo, Ningjing Chen, Shigang Li, Shuixiu Xia, Jie Chen, Dawei Li, Lubo Zhang and Zhice Xu
Intrauterine environments are related to fetal renal development and postnatal health. Influence of salty diets during pregnancy on renal functions and renin–angiotensin system (RAS) was determined in the ovine fetuses and offspring. Pregnant ewes were fed high-salt diet (HSD) or normal-salt diet (NSD) for 2 months during middle-to-late gestation. Fetal renal functions, plasma hormones, and mRNA and protein expressions of the key elements of renal RAS were measured in the fetuses and offspring. Fetal renal excretion of sodium was increased while urine volume decreased in the HSD group. Fetal blood urea nitrogen was increased, while kidney weight:body weight ratio decreased in the HSD group. The altered ratio was also observed in the offspring aged 15 and 90 days. Maternal and fetal plasma antidiuretic hormone was elevated without changes in plasma renin activity and Ang I levels, while plasma Ang II was decreased. The key elements of local renal RAS, including angiotensinogen, angiotensin converting enzyme (ACE), ACE2, AT1, and AT2 receptor expression in both mRNA and protein, except renin, were altered following maternal high salt intake. The results suggest that high intake of salt during pregnancy affected fetal renal development associated with an altered expression of the renal key elements of RAS, some alterations of fetal origins remained after birth as possible risks in developing renal or cardiovascular diseases.