title: Chronic high-fat diet increases acute neuroendocrine stress response independently of prenatal dexamethasone treatment in male rats.
abstract: OBJECTIVE
  Intrauterine growth restriction (IUGR) has been associated with metabolic disorders later in life such as obesity and diabetes as well as psychiatric disorders such as depression and schizophrenia. Therefore, we wanted to investigate whether behavioural, metabolic or neuroendocrine abnormalities could be provoked or exacerbated by a high-fat diet (HFD) in an experimental model of IUGR.
  
  
  METHODS
  Pregnant dams were exposed to dexamethasone (DEX) in the third gestational week to induce IUGR. Late adolescent male offspring of DEX- and vehicle-treated dams were then fed a HFD or standard chow for 8 weeks and subjected to a variety of assessments.
  
  
  RESULTS
  Only diet affected the hypothalamus-pituitary-adrenal (HPA) axis stress response, as HFD doubled the observed corticosterone levels following acute restraint. HFD and prenatal DEX exposure concomitantly exacerbated depressive-like behaviour in the forced swim test, even though no interaction was seen. Prenatal DEX treatment tended to increase the basal acoustic startle response (ASR), while an interaction between HFD and DEX was present in the ASR pre-pulse inhibition suggestive of fundamental changes in neuronal gating mechanisms. Metabolic parameters were only affected by diet, as HFD increased fasting glucose and insulin levels.
  
  
  CONCLUSIONS
  We conclude that chronic HFD may be more important in programming of the HPA axis stress responsiveness than an adverse foetal environment and therefore potentially implies an increased risk for developing psychiatric and metabolic disease.
authors.affiliation: 1 Translational Neuropsychiatry Unit, Aarhus University, Risskov, Denmark.
authors.forename: Anders
authors.initials: A
authors.lastname: Abildgaard
authors.affiliation: 2 Medical Department MEA (endocrinology), Aarhus University Hospital, Aarhus, Denmark.
authors.forename: Sten
authors.initials: S
authors.lastname: Lund
authors.affiliation: 3 National Research Centre for the Working Environment, Copenhagen, Denmark.
authors.forename: Karin S
authors.initials: KS
authors.lastname: Hougaard
mesh_terms: D000818:Animals; D001786:Blood Glucose; D003345:Corticosterone / Q000097:blood; D003863:Depression / Q000378:metabolism; D003907:Dexamethasone / Q000633:toxicity; D059305:Diet, High-Fat; D004195:Disease Models, Animal; D005260:Female; D005317:Fetal Growth Retardation / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology*; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D008297:Male; D009043:Motor Activity / Q000502:physiology; D010913:Pituitary-Adrenal System / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological
chemical_list: D001786:Blood Glucose; D007328:Insulin; D003907:Dexamethasone; D003345:Corticosterone