title: Maternal obesity and high-fat diet program offspring metabolic syndrome.
abstract: OBJECTIVE
  We determined the potential programming effects of maternal obesity and high-fat (HF) diet during pregnancy and/or lactation on offspring metabolic syndrome.
  
  
  METHODS
  A rat model of maternal obesity was created using an HF diet prior to and throughout pregnancy and lactation. At birth, pups were cross-fostered, thereby generating 4 paradigms of maternal diets during pregnancy/lactation: (1) control (Con) diet during pregnancy and lactation (Con/Con), (2) HF during pregnancy and lactation (HF/HF), (3) HF during pregnancy alone (HF/Con), and (4) HF during lactation alone (Con/HF).
  
  
  RESULTS
  Maternal phenotype during pregnancy and the end of lactation evidenced markedly elevated body fat and plasma corticosterone levels in HF dams. In the offspring, the maternal HF diet during pregnancy alone programmed increased offspring adiposity, although with normal body weight, whereas the maternal HF diet during lactation increased both body weight and adiposity. Metabolic disturbances, particularly that of hyperglycemia, were apparent in all groups exposed to the maternal HF diet (during pregnancy and/or lactation), although differences were apparent in the manifestation of insulin resistant vs insulin-deficient phenotypes. Elevated systolic blood pressure was manifest in all groups, implying that exposure to an obese/HF environment is disadvantageous for offspring health, regardless of pregnancy or lactation periods. Nonetheless, the underlying mechanism may differ because offspring that experienced in utero HF exposure had increased corticosterone levels.
  
  
  CONCLUSIONS
  Maternal obesity/HF diet has a marked impact on offspring body composition and the risk of metabolic syndrome was dependent on the period of exposure during pregnancy and/or lactation.
authors.affiliation: Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Department of Obstetrics and Gynecology, Perinatal Research Laboratories, Torrance, CA; Department of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles, CA. Electronic address: mdesai@obgyn.humc.edu.
authors.forename: Mina
authors.initials: M
authors.lastname: Desai
authors.affiliation: Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Department of Obstetrics and Gynecology, Perinatal Research Laboratories, Torrance, CA.
authors.forename: Juanita K
authors.initials: JK
authors.lastname: Jellyman
authors.affiliation: Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Department of Obstetrics and Gynecology, Perinatal Research Laboratories, Torrance, CA.
authors.forename: Guang
authors.initials: G
authors.lastname: Han
authors.affiliation: Los Angeles Perinatal Association, Los Angeles, CA.
authors.forename: Marie
authors.initials: M
authors.lastname: Beall
authors.affiliation: Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI.
authors.forename: Robert H
authors.initials: RH
authors.lastname: Lane
authors.affiliation: Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Department of Obstetrics and Gynecology, Perinatal Research Laboratories, Torrance, CA; Department of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles, CA.
authors.forename: Michael G
authors.initials: MG
authors.lastname: Ross
mesh_terms: D000818:Animals; D001823:Body Composition; D003345:Corticosterone / Q000097:blood; D059305:Diet, High-Fat; D004435:Eating; D005260:Female; D007774:Lactation; D008055:Lipids / Q000097:blood; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D024821:Metabolic Syndrome / Q000209:etiology*; D009765:Obesity / Q000150:complications*; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D008055:Lipids; D003345:Corticosterone
keywords: hypertension; impaired glucose tolerance; lactation; obesity; pregnancy; rat