Iron deficiency in pregnancy: Influence on sleep, behavior, and molecular markers of adult male offspring.

Iron restriction during pregnancy can lead to iron deficiency and changes in the dopaminergic system in the adulthood of offspring, and restless legs syndrome (RLS) is closely related to these changes. Objectives: Analyze whether iron restriction during pregnancy would cause changes in the behavior, sleep, and dopaminergic system of the male offspring. In addition, we aimed to assess whether exercise would be able to modulate these variables. The pregnant rats (Wistar) were divided into four groups with different concentrations of iron in the diet: standard (St), supplementation (Su), restriction since weaning (R1), and restriction only during pregnancy (R2). After birth, the offspring were assigned to their respective groups according to the dams diet (St, Su, R1, and R2) and distributed into sedentary (SD) and exercised (EX) (for 8 weeks of training), reaching eight groups of offspring (O): OSt SD, OSt EX, OSu SD, OSu EX, OR1 SD, OR1 EX, OR2 SD, and OR2 EX. Sleep, behavior, and analysis of key genes of dopaminergic system (D2, DAT) were performed after 8 weeks. The results for trained offspring that the mother received supplementation diet were the most expressive, with increased freezing and the OR1 SD group showed an increase in DAT protein content. These changes may have been due to the association between the dams diet during pregnancy and the practice of exercise by the offspring. The different concentrations of iron during pregnancy caused changes in the offspring, however, they were not associated with fetal programming in the context of RLS.

Early life nicotine exposure alters mRNA and microRNA expressions related to thyroid function and lipid metabolism in liver and BAT of adult wistar rats.

In rats, maternal nicotine exposure during lactation induces obesity, thyroid dysfunction, brown adipose tissue (BAT) hypofunction and liver alterations in adult offspring. Both thyroid function and lipid metabolism are influenced by gene silencing mediated by microRNAs (miRNAs). Here we investigated long-term effects of early nicotine exposure on molecular and epigenetic mechanisms closely related to thyroid and lipid metabolism, through the expression of mRNAs and miRNAs in BAT and liver of adult male and female offspring. At postnatal day 2 (PND2), lactating control (CON) or nicotine (NIC) dams were subcutaneously implanted with osmotic minipumps containing, respectively, saline or 6 mg/kg nicotine. Litters were adjusted to 3 males and 3 females. Offspring's euthanasia occurred at PND180. In the BAT, NIC females showed higher Dio2 mRNA expression, while miR-382* expression was not altered in both sexes. In the liver, NIC offspring of both sexes showed lower Dio1 mRNA expression and higher miR-224 expression, while only NIC females had higher miR-383 and miR-21 expressions. NIC offspring of both sexes showed higher mRNA expression of SCD1 in the liver; NIC males had decreased CPT1 expression, whereas NIC females had increased FASN, miR-370 and miR-122 expressions. Regardless of sex, alterations in liver Dio1, miR-224 and SCD1 expressions are involved in the disturbances caused by maternal nicotine exposure during breastfeeding. Interestingly, females had more altered miRs in the liver. Early nicotine exposure induces a sex dimorphism, particularly regarding hepatic lipid metabolism, through miRs expression.