A post-weaning fish oil dietary intervention reverses adverse metabolic outcomes and 11β-hydroxysteroid dehydrogenase type 1 expression in postnatal overfed rats

Br J Nutr. 2016 Nov;116(9):1519-1529. doi: 10.1017/S0007114516003718. Epub 2016 Nov 7.

Abstract

Early life is considered a critical period for determining long-term metabolic health. Postnatal over-nutrition may alter glucocorticoid (GC) metabolism and increase the risk of developing obesity and metabolic disorders in adulthood. Our aim was to assess the effects of the dose and timing of a fish oil diet on obesity and the expression of GC-activated enzyme 11β-hydroxysteroid dehydrogenase type 1 (HSD1) in postnatal overfed rats. Litter sizes were adjusted to three (small litter (SL)) or ten (normal litter) rats on postnatal day 3 to induce overfeeding or normal feeding. The SL rats were divided into three groups after weaning: high-dose fish oil (HFO), low-dose fish oil (LFO) and standard-diet groups. After 10 weeks, the HFO diet reduced body weight gain (16 %, P0·05). In conclusion, the post-weaning HFO diet could reverse adverse outcomes and decrease tissue GC activity in postnatal overfed rats.

Keywords: n-3 PUFA; 11β-HSD1 11β-hydroxysteroid dehydrogenase type 1; C/EBPα CCAAT/enhancer-binding protein α; GC glucocorticoid; HFO high-dose fish oil; IPGTT intraperitoneal glucose tolerance test; LFO low-dose fish oil; NL normal litter; SL small litter; TC total cholesterol; 11β-Hydroxysteroid dehydrogenase type 1; Obesity; Postnatal overfeeding.

MeSH terms

  • 11-beta-Hydroxysteroid Dehydrogenase Type 1 / genetics
  • 11-beta-Hydroxysteroid Dehydrogenase Type 1 / metabolism*
  • Adipose Tissue, White / enzymology*
  • Adipose Tissue, White / metabolism
  • Adipose Tissue, White / pathology
  • Adiposity
  • Animals
  • Anti-Obesity Agents / administration & dosage
  • Anti-Obesity Agents / therapeutic use
  • Cell Size
  • Dietary Supplements*
  • Disease Models, Animal*
  • Fish Oils / administration & dosage
  • Fish Oils / therapeutic use*
  • Gene Expression Regulation, Developmental*
  • Glucose Intolerance / etiology
  • Glucose Intolerance / prevention & control
  • Hyperlipidemias / etiology
  • Hyperlipidemias / prevention & control
  • Lipid Metabolism
  • Liver / enzymology
  • Liver / metabolism
  • Male
  • Metabolic Syndrome / etiology
  • Metabolic Syndrome / metabolism
  • Metabolic Syndrome / pathology
  • Metabolic Syndrome / prevention & control*
  • Overnutrition / physiopathology
  • RNA, Messenger / metabolism
  • Random Allocation
  • Rats, Sprague-Dawley
  • Weaning
  • Weight Gain

Substances

  • Anti-Obesity Agents
  • Fish Oils
  • RNA, Messenger
  • 11-beta-Hydroxysteroid Dehydrogenase Type 1