Dexamethasone reduces energy expenditure and increases susceptibility to diet-induced obesity in mice.
basic_science · Level V
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- Record sourced from PubMed, PMID 23408649.
- Also identified by DOI 10.1002/oby.20338 and PMC identifier 4451231.
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Abstract
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). 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. 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. 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.
Medical subject headings
- Adipose Tissue
- Dexamethasone
- Diet, High-Fat
- Energy Metabolism
- Glucocorticoids
- Obesity
- Thermogenesis