title: Prenatal exposure to lipopolysaccharide results in local RAS activation in the adipose tissue of rat offspring.
abstract: BACKGROUND
  Adult metabolic syndrome may originate in part during fetal or early life. This study was designed to investigate the effects of prenatal exposure to lipopolysaccharide (LPS) on adipose development and local renin-angiotensin system (RAS) activation in rat offspring.
  
  
  METHODS
  Pregnant rats were randomly divided into three groups (n = 8 in each), including an NS group (pregnant rats were only treated with 0.5 ml normal saline from the 8th to the 14th day of gestation); an LPS group (pregnant rats were injected intraperitoneally with 0.79 mg/kg LPS on the 8th, 10th and 12th days of pregnancy); and an LPS+pyrrolidine dithiocarbamate (PDTC) group (identical to the LPS group except that 100 mg/kg PDTC was administered from the 8th to the 14th day of gestation).
  
  
  RESULTS
  Prenatal exposure to LPS resulted in increased blood pressure, adipose coefficient and body weight in rat offspring. Specifically, during the infancy of the offspring rats, the LPS stimulus promoted the differentiation of adipose cells, diminishing their diameters and proportions while simultaneously increasing cell number. In contrast, once the rats were grown, adipose cell differentiation was inhibited, and the diameters and proportions of the cells were increased. Moreover, each component of the RAS was changed and was shown to be activated. PDTC, an inhibitor of NF-κB, could reverse the influence of the stimulus during pregnancy.
  
  
  CONCLUSIONS
  Prenatal exposure to LPS in rats results in increased blood pressure, adipose coefficient, body weight and activation of adipose RAS in offspring.
authors.affiliation: Institute of Materia Medical, College of Pharmacy, Third Military Medical University, Chongqing, China.
authors.forename: Meng
authors.initials: M
authors.lastname: Gao
authors.affiliation: Department of Medicament and Instrument, 159 Hospital of PLA, Zhumadian, Henan, China.
authors.forename: Xingxing
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Institute of Materia Medical, College of Pharmacy, Third Military Medical University, Chongqing, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Chen
authors.affiliation: Institute of Materia Medical, College of Pharmacy, Third Military Medical University, Chongqing, China.
authors.forename: Cunyun
authors.initials: C
authors.lastname: Mi
authors.affiliation: Institute of Materia Medical, College of Pharmacy, Third Military Medical University, Chongqing, China.
authors.forename: Yujie
authors.initials: Y
authors.lastname: Tang
authors.affiliation: Institute of Materia Medical, College of Pharmacy, Third Military Medical University, Chongqing, China.
authors.forename: Jianzhi
authors.initials: J
authors.lastname: Zhou
authors.affiliation: Institute of Materia Medical, College of Pharmacy, Third Military Medical University, Chongqing, China.
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Li
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002454:Cell Differentiation / Q000187:drug effects; D048429:Cell Size / Q000187:drug effects; D005260:Female; D005951:Glucose Tolerance Test; D008070:Lipopolysaccharides / Q000494:pharmacology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System / Q000187:drug effects*
chemical_list: D015415:Biomarkers; D008070:Lipopolysaccharides; D012333:RNA, Messenger