Maternal malnutrition lead to the incidence of metabolic diseases in offspring. The purpose of this project was to exam whether maternal low chromium could disturb normal lipid metabolism in offspring, altering adipose cell differentiation and leading the incidence of lipid metabolism diseases, including metabolic syndrome and obesity. Female C57BL mice were given a control diet (CD) or a low chromium diet (LCD) during the gestational and lactation periods. After weaning, offspring was fed with CD or LCD. The female offspring were assessed at 32 weeks of age. Fresh adipose samples from CD-CD group and LCD-CD group were collected. Genome mRNA were analyzed using Affymetrix GeneChip Mouse Gene 2.0 ST Whole Transcript-based Array. Differently expressed genes were analyzed based on Gene Ontology and KEGG pathway analysis database. Maternal low chromium irreversibly increased offspring body weight, fat pad weight, serum TG and TNF-α. Eighty-five genes increased and 109 genes reduced in the offspring adipose of the maternal low chromium group. According to KEGG pathway and String analyses, the PPAR signaling pathway may be a key controlled pathway related to the effect of maternal low chromium on female offspring. Maternal chromium status have long-term effects of lipid metabolism in female mice offspring. Normalizing offspring diet can't reverse these effects. The potential underlying mechanisms are the disturbance of the PPAR signaling pathway in adipose tissue.
- gene expression
- lipid metabolism
- PPAR pathway
- ©2017 The Author(s)
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