title: The timing of nutrient restriction during rat pregnancy/lactation alters metabolic syndrome phenotype.
abstract: OBJECTIVE
  Modulation of growth of intrauterine growth restricted (IUGR) newborns causes either adult obesity or normalization of body weight and fat. We investigated the impact of rapid versus delayed catch-up growth of IUGR offspring on glucose and lipid profiles.
  
  
  METHODS
  From 10 days to term gestation and through lactation, control pregnant rats received ad libitum food, whereas study rats were 50% food restricted. Cross-fostering techniques were used to examine effects of food restriction during pregnancy and/or lactation periods. Glucose and lipid profiles were determined in offspring at ages 1 day, 3 weeks, and 9 months.
  
  
  RESULTS
  Food restriction during pregnancy produced hypoglycemic IUGR pups. Those permitted rapid catch-up growth demonstrated adult obesity with insulin resistance (hyperglycemia/hyperinsulinemia) and hypertriglyceridemia. Conversely, IUGR exhibiting delayed catch-up growth demonstrated normal adult body weight and insulin deficiency (hyperglycemia/hypoinsulinemia) and elevated cholesterol levels as compared with controls. However, these adult offspring had higher glucose though similar insulin levels as control offspring nursed by food restricted dam.
  
  
  CONCLUSIONS
  The timing and the rate of IUGR newborn catch-up growth causes markedly altered adult phenotypes. Although delayed newborn catch-up growth may be beneficial in the prevention of adult obesity, there may be significant adverse effects on pancreatic function.
authors.affiliation: Department of Obstetrics and Gynecology, David-Geffen School of Medicine at University of California, Los Angeles, CA, USA. mdesai@obgyn.humc.edu
authors.forename: Mina
authors.initials: M
authors.lastname: Desai
authors.forename: Dave
authors.initials: D
authors.lastname: Gayle
authors.forename: Jooby
authors.initials: J
authors.lastname: Babu
authors.forename: Michael G
authors.initials: MG
authors.lastname: Ross
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001786:Blood Glucose / Q000032:analysis; D002784:Cholesterol / Q000097:blood; D005247:Feeding Behavior / Q000502:physiology; D005260:Female; D005317:Fetal Growth Retardation / Q000178:diet therapy / Q000503:physiopathology*; D005508:Food Deprivation / Q000502:physiology*; D006943:Hyperglycemia / Q000503:physiopathology; D015228:Hypertriglyceridemia / Q000503:physiopathology; D007003:Hypoglycemia / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology; D007774:Lactation / Q000502:physiology*; D008099:Liver / Q000473:pathology; D008297:Male; D024821:Metabolic Syndrome / Q000503:physiopathology*; D009929:Organ Size; D010179:Pancreas / Q000473:pathology; D010641:Phenotype; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012737:Sex Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D007328:Insulin; D014280:Triglycerides; D002784:Cholesterol