title: PPARγ links maternal malnutrition and abnormal glucose and lipid metabolism in the offspring of mice.
abstract: Peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptor proteins that regulate gene transcription. PPARs play essential roles in modulating cell differentiation, development, and metabolism (carbohydrate, lipid, protein). Here, we investigated whether PPARγ plays a role in linking maternal malnutrition and aberrant metabolism in the offspring of mice. After feeding dams with high fat (HF) and low protein (LP) diet during pregnancy and lactation, we examined the effects on the offspring at weaning (age of 3-week). The results showed that the LP offspring had lower body weight and length than the control. The HF offspring had heavier body weight and longer body length than LP. The blood glucose levels in HF group were significantly higher at 30 min and 60 min after intraperitoneal glucose administration and the area under curve was also significantly larger than the control. The blood glucose levels in HF group were significantly higher at 30 min than LP. HF group had elevated total cholesterol levels and LP group had decreased total cholesterol levels compared with the control. All results were statistically significant as examined by t-test. More importantly, PPARγ expression levels detected by qRT-PCR were significantly increased in HF and LP groups compared with the control. In conclusion, maternal HF and LP diet during pregnancy and lactation can induce impaired glucose and lipid metabolism in the early life of mouse offspring, where PPARγ may play an important role.
authors.affiliation: Key Laboratory of Endocrinology of Ministry of Health; Department of Endocrinology, Peking Union Medical College Hospital; Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Zheng
authors.affiliation: Key Laboratory of Endocrinology of Ministry of Health; Department of Endocrinology, Peking Union Medical College Hospital; Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
authors.forename: Xin-Hua
authors.initials: XH
authors.lastname: Xiao
authors.affiliation: Key Laboratory of Endocrinology of Ministry of Health; Department of Endocrinology, Peking Union Medical College Hospital; Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Zhang
authors.affiliation: Key Laboratory of Endocrinology of Ministry of Health; Department of Endocrinology, Peking Union Medical College Hospital; Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
authors.forename: Miao
authors.initials: M
authors.lastname: Yu
authors.affiliation: Key Laboratory of Endocrinology of Ministry of Health; Department of Endocrinology, Peking Union Medical College Hospital; Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
authors.forename: Jian-Ping
authors.initials: JP
authors.lastname: Xu
authors.affiliation: Key Laboratory of Endocrinology of Ministry of Health; Department of Endocrinology, Peking Union Medical College Hospital; Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
authors.forename: Zhi-Xin
authors.initials: ZX
authors.lastname: Wang
authors.affiliation: Key Laboratory of Endocrinology of Ministry of Health; Department of Endocrinology, Peking Union Medical College Hospital; Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
authors.forename: Yi-Jing
authors.initials: YJ
authors.lastname: Liu
authors.affiliation: Key Laboratory of Endocrinology of Ministry of Health; Department of Endocrinology, Peking Union Medical College Hospital; Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China.
authors.forename: Ming-Min
authors.initials: MM
authors.lastname: Li
mesh_terms: D000821:Animal Feed / Q000032:analysis; D000818:Animals; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D050356:Lipid Metabolism; D008297:Male; D044342:Malnutrition / Q000235:genetics / Q000378:metabolism*; D039382:Maternal Nutritional Physiological Phenomena; D051379:Mice; D008810:Mice, Inbred C57BL; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000235:genetics / Q000378:metabolism*; D014886:Weaning
chemical_list: D047495:PPAR gamma; D005947:Glucose