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地塞米松可降低小鼠的能量消耗,并增加其对饮食诱导肥胖的易感性。

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

机构信息

Division of Endocrinology Diabetes and Metabolism, University of Miami Miller School of Medicine, Miami, Florida, USA.

出版信息

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.

摘要

目的

研究长期使用地塞米松对小鼠能量消耗和肥胖的影响,以及这是否受高脂饮食(HFD)喂养的影响。

设计与方法

将小鼠置于 HFD 中 2 周,然后在接下来的 7 周内每隔一天用 5mg/kg 的地塞米松进行治疗。

结果

地塞米松治疗会增加体脂肪,这一效果在 HFD 喂养的动物中更为明显;地塞米松治疗还加重了 HFD 引起的肝脂肪变性。与此同时,地塞米松治疗降低了 HFD 喂养动物的呼吸商,并减缓了这些动物夜间的代谢率。此外,由于观察到这些动物的棕色脂肪组织中 UCP-1mRNA 的显著减少,β3 肾上腺素能刺激引起的急性 VO2 加速明显受到限制。

结论

在饮食诱导肥胖的小鼠模型中,长期使用地塞米松治疗会降低棕色脂肪组织的产热作用,并加剧肥胖和肝脂肪变性。©2013 美国化学工程师学会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d31c/4451231/144da840dc05/nihms434493f1.jpg

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