Abstract
It is now broadly accepted that the nutritional environment in early life is a key factor in susceptibility to metabolic diseases. In this study, we evaluated the effects of maternal chromium restriction in vivo on the modulation of lipid metabolism and the mechanisms involved in this process. Sixteen pregnant C57BL mice were randomly divided into two dietary treatments: a control (C) diet group and a low chromium (L) diet group. The diet treatment was maintained through gestation and lactation period. After weaning, some of the pups continued with either the control diet or low chromium diet (CC or LL), whereas other pups switched to another diet (CL or LC). At 32 weeks of age, serum lipid metabolism, proinflammatory indexes, oxidative stress and anti-oxidant markers, and DNA methylation status in adipose tissue were measured. The results indicated that the maternal low chromium diet increased body weight, fat pad weight, serum triglyceride (TG), low-density lipoprotein cholesterol (LDL), tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), and oxidized glutathione (GSSG). There was a decrease in serum reduced/oxidized glutathione (GSH/GSSG) ratio at 32 weeks of age in female offspring. From adipose tissue, we identified 1214 individual hypomethylated CpG sites and 411 individual hypermethylated CpG sites in the LC group when compared to the CC group. Pathway analysis of the differential methylation genes revealed a significant increase in hypomethylated genes in the mitogen-activated protein kinase (MAPK) signaling pathway in the LC group. Our study highlights the importance of the MAPK signaling pathway in epigenetic changes involved in the lipid metabolism of the offspring from chromium-restricted dams.
Highlights
Studies have implied that nutrition during fetal and neonatal life can have profound effects on lifespan, glucose, and lipid metabolism
The results showed that the LC group had significantly high expression levels of Map3k4, Map3k5, Mapk14, the kinase 1/MAP3K7 binding binding protein 2protein (Tab2), Atf2, and Pparg compared to CC group (p < 0.01, Figure 6f)
Our research found that maternal chromium restriction increased serum MDA level and reduced GSH/GSSG ratio in offspring
Summary
Studies have implied that nutrition during fetal and neonatal life can have profound effects on lifespan, glucose, and lipid metabolism. Human studies conducted in 1944–1945 revealed that undernutrition during early pregnancy was associated with glucose intolerance and increased serum insulin concentrations later in life (50–58 years-old) [1]. It was the first time that scientists addressed the impact of adverse environmental factors in early life on the occurrence of metabolic diseases in Nutrients 2016, 8, 488; doi:10.3390/nu8080488 www.mdpi.com/journal/nutrients. One important mechanism believed to be involved in this relationship is DNA methylation. DNA methylation changes normally occur within CpG-rich regions (CpG islands). CpG islands are usually located near the promoter regions of genes. Methylation within the promoter region can negatively affect gene expression [5]
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