title: Gender-specific programmed hepatic lipid dysregulation in intrauterine growth-restricted offspring.
abstract: OBJECTIVE
  Intrauterine growth restriction demonstrates increased risk of adult metabolic syndrome. The associated hyperlipidemia results from obesity or programmed metabolic abnormalities. Because lipid homeostasis is regulated by the liver, we hypothesized that hepatic structure and lipid content in intrauterine growth restriction would reflect a primary lipid dysfunction.
  
  
  METHODS
  From 10 days to term gestation, control pregnant rats received ad libitum diet; study rats were 25% food-restricted (FR). All dams received ad libitum diet throughout lactation. At 3 weeks of age, hepatic lobule size and lipid profile of the pups were determined.
  
  
  RESULTS
  At 3 weeks of age, body and liver weights of the pups were comparable with controls, although with reduced hepatic lobule size. FR males had increased hepatic triglyceride and cholesterol content with elevated sterol regulatory element-binding protein-1c, fatty acid synthase, and lipoprotein lipase expression; FR females exhibited decreased hepatic cholesterol levels. Plasma lipid levels were unchanged in FR males and females.
  
  
  CONCLUSIONS
  Developmental programming results in sex-dependent altered lipid metabolism with increased risk in males.
authors.affiliation: Los Angeles Biomedical Research Institute at Harbor-University of California Los Angeles Medical Center, Torrance, CA, USA.
authors.forename: Gyu Yeon
authors.initials: GY
authors.lastname: Choi
authors.forename: Darran N
authors.initials: DN
authors.lastname: Tosh
authors.forename: Ambica
authors.initials: A
authors.lastname: Garg
authors.forename: Roy
authors.initials: R
authors.lastname: Mansano
authors.forename: Michael G
authors.initials: MG
authors.lastname: Ross
authors.forename: Mina
authors.initials: M
authors.lastname: Desai
mesh_terms: D000818:Animals; D002784:Cholesterol / Q000032:analysis; D004032:Diet / Q000009:adverse effects; D004195:Disease Models, Animal; D050171:Dyslipidemias / Q000097:blood / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D064429:Fatty Acid Synthases / Q000096:biosynthesis; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology / Q000503:physiopathology*; D050356:Lipid Metabolism / Q000502:physiology*; D008071:Lipoprotein Lipase / Q000378:metabolism; D008099:Liver / Q000737:chemistry / Q000473:pathology*; D008297:Male; D009929:Organ Size; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000503:physiopathology*; D039401:Prenatal Nutritional Physiological Phenomena; D051381:Rats; D017207:Rats, Sprague-Dawley; D012737:Sex Factors; D051780:Sterol Regulatory Element Binding Protein 1 / Q000096:biosynthesis; D014280:Triglycerides / Q000032:analysis
chemical_list: C497387:SREBF1 protein, human; D051780:Sterol Regulatory Element Binding Protein 1; D014280:Triglycerides; D002784:Cholesterol; D064429:Fatty Acid Synthases; D008071:Lipoprotein Lipase