The Development of Metabolic Derangement in Male Offspring after Perinatal Exposure to Di-(2-Ethylhexyl) Phthalate

The prevalence of obesity and type 2 diabetes mellitus（T2DM）has been increasing throughout the world over the past 20 years.Environmental chemicals known to regulate the endocrine system have been considered as a risk factor for the development of metabolic diseases.Several people are exposed to environmental chemicals during their lives.

Assessing pre/post-weaning neurobehavioral development for perinatal exposure to low doses of methylmercury

Fetuses and neonates are known to be high-risk groups for Methylmercury（MeHg）exposure.MeHg can be transferred to the fetus through the placenta and to newborn offspring through breast milk.The aim of the present study was to investigate the neurotoxic effects of low doses of MeHg（1 and 5 μg/m L in drinking water） administration,from gestational day 1 to postnatal day（PND） 21,on the neurobehavioral development of rats.The results showed that the no-observed-effect level of MeHg is somewhere in the range of 1-4 μg/mL.Neurobehavioral development analysis revealed a delayed appearance of cliff drop and negative geotaxis reflexes in the 5 μg/mL MeHg exposure group.Developmental exposure to MeHg affected locomotor activity functions for the females,but not for the males,implying that the female pups were more vulnerable than the male pups.All pups exposed to 5 μg/mL of MeHg showed a significant deficit in motor coordination in the rotarod test compared with controls,and the highest accumulated concentrations of Hg were found in the cerebellum,followed by the hippocampus and cerebral cortex,indicating that the cerebellum is a possible target for MeHg toxicity.We demonstrated adverse effects of developmental exposure to MeHg associated with tissue concentrations very close to the current human body burden of this persistent and bioaccumulative compound.

Effect of Perinatal Bisphenol A Exposure on Serum Lipids and Lipid Enzymes in Offspring Rats of Different Sex

Rats were exposed to1 or 10 μg/mL bisphenol A （BPA） in water during pregnancy and lactation. Offspring rats were given normal water and a standard diet from weaning to postnatal day （PND） 50. Perinatal exposure to BPA resulted in significantly increased body weight, visceral adipose tissue, abnormal serum lipids, and lower adiponectin （ADP） levels in both female and male offspring rats. Liver adipose triglyceride lipase （Atgl） mRNA levels and ADP protein in visceral adipose tissue were significantly decreased in BPA-exposed offspring rats. In both female or male offspring rats, obesity and dyslipidemia induced by perinatal exposure to BPA were associated with down regulation of Atgl mRNA in liver and ADP protein in visceral adipose tissue.

Early exposure to food contaminants reshapes maturation of the human brain-gut-microbiota axis

Early childhood growth and development is conditioned by the consecutive events belonging to perinatal programming. This critical window of life will be very sensitive to any event altering programming of the main body functions.Programming of gut function, which is starting right after conception, relates to a very well-established series of cellular and molecular events associating all types of cells present in this organ, including neurons, endocrine and immune cells. At birth, this machinery continues to settle with the establishment of extra connection between enteric and other systemic systems and is partially under the control of gut microbiota activity, itself being under the densification and the diversification of microorganisms’ population. As thus, any environmental factor interfering on this pre-established program may have a strong incidence on body functions. For all these reasons, pregnant women, fetuses and infants will be particularly susceptible to environmental factors and especially food contaminants. In this review, we will summarize the actual understanding of the consequences of repeated low-level exposure to major food contaminants on gut homeostasis settlement and on brain/gut axis communication considering the pivotal role played by the gut microbiota during the fetal and postnatal stages and the presumed consequences of these food toxicants on the individuals especially in relation with the risks of developing later in life non-communicable chronic diseases.