Dexamethasone reduces energy expenditure and increases susceptibility to diet-induced obesity in mice

Obesity (Silver Spring). 2013 Sep;21(9):E415-20. doi: 10.1002/oby.20338.

Abstract

Objective: To investigate how long-term treatment with dexamethasone affects energy expenditure and adiposity in mice and whether this is influenced by feeding on a high-fat diet (HFD).

Design and methods: Mice were placed on a HFD for 2 weeks and started on dexamethasone at 5 mg/kg every other day during the next 7 weeks.

Results: Treatment with dexamethasone increased body fat, an effect that was more pronounced in the animals kept on HFD; dexamethasone treatment also worsened liver steatosis caused by the HFD. At the same time, treatment with dexamethasone lowered the respiratory quotient in chow-fed animals and slowed nightly metabolic rate in the animals kept on HFD. In addition, the acute VO2 acceleration in response to β3 adrenergic-stimulation was significantly limited in the dexamethasone-treated animals, as a result of marked decrease in UCP-1 mRNA observed in the brown adipose tissue of these animals.

Conclusions: Long-term treatment with dexamethasone in a mouse model of diet-induced obesity decreases brown adipose tissue thermogenesis and exaggerates adiposity and liver steatosis. © 2013 American Institute of Chemical Engineers AIChE J, 2013.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adipose Tissue / drug effects*
  • Adipose Tissue / metabolism
  • Adipose Tissue, Brown / metabolism
  • Adiposity / drug effects
  • Animals
  • Basal Metabolism / drug effects
  • Dexamethasone / adverse effects*
  • Dexamethasone / pharmacology
  • Diet, High-Fat / adverse effects*
  • Dietary Fats / administration & dosage
  • Disease Models, Animal
  • Energy Metabolism / drug effects*
  • Fatty Liver / etiology
  • Glucocorticoids / adverse effects*
  • Glucocorticoids / pharmacology
  • Ion Channels / genetics
  • Ion Channels / metabolism
  • Liver / drug effects
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mitochondrial Proteins / genetics
  • Mitochondrial Proteins / metabolism
  • Obesity / etiology*
  • Obesity / genetics
  • Obesity / metabolism
  • Oxygen Consumption / drug effects
  • RNA, Messenger / metabolism
  • Respiration / drug effects
  • Thermogenesis / drug effects*
  • Uncoupling Protein 1

Substances

  • Dietary Fats
  • Glucocorticoids
  • Ion Channels
  • Mitochondrial Proteins
  • RNA, Messenger
  • Ucp1 protein, mouse
  • Uncoupling Protein 1
  • Dexamethasone