The effect of maternal chromium status on lipid metabolism in female elderly mice offspring and involved molecular mechanism.
Maternal malnutrition leads to the incidence of metabolic diseases in offspring. The purpose of this project was to examine whether maternal low chromium could disturb normal lipid metabolism in offspring, altering adipose cell differentiation and leading to 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 analysed using Affymetrix GeneChip Mouse Gene 2.0 ST Whole Transcript-based array. Differentially expressed genes (DEGs) were analysed based on gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis database. Maternal low chromium irreversibly increased offspring body weight, fat-pad weight, serum triglyceride (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 signalling pathway may be the 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 not reverse these effects. The potential underlying mechanisms are the disturbance of the PPAR signalling pathway in adipose tissue.
Key Laboratory of Endocrinology, Translational Medicine Centre, Ministry of Health, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Qian
Q
Zhang
Department of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.
Xiaofang
X
Sun
Key Laboratory of Endocrinology, Translational Medicine Centre, Ministry of Health, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China xiaoxh2014@vip.163.com.
Xinhua
X
Xiao
Key Laboratory of Endocrinology, Translational Medicine Centre, Ministry of Health, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Jia
J
Zheng
Key Laboratory of Endocrinology, Translational Medicine Centre, Ministry of Health, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Ming
M
Li
Key Laboratory of Endocrinology, Translational Medicine Centre, Ministry of Health, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Miao
M
Yu
Key Laboratory of Endocrinology, Translational Medicine Centre, Ministry of Health, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Fan
F
Ping
Key Laboratory of Endocrinology, Translational Medicine Centre, Ministry of Health, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Zhixin
Z
Wang
Key Laboratory of Endocrinology, Translational Medicine Centre, Ministry of Health, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Cuijuan
C
Qi
Key Laboratory of Endocrinology, Translational Medicine Centre, Ministry of Health, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Tong
T
Wang
Key Laboratory of Endocrinology, Translational Medicine Centre, Ministry of Health, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Xiaojing
X
Wang
D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D000831:Animals, Newborn; D001835:Body Weight; D002857:Chromium / Q000097:blood / Q000378:metabolism*; D004032:Diet / Q000009:adverse effects; D005260:Female; D005786:Gene Expression Regulation; D050356:Lipid Metabolism; D052439:Lipid Metabolism Disorders / Q000097:blood / Q000209:etiology* / Q000235:genetics / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D047492:Peroxisome Proliferator-Activated Receptors / Q000235:genetics / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction
D047492:Peroxisome Proliferator-Activated Receptors; D002857:Chromium
PPAR pathway; chromium; development; gene expression; lipid metabolism