1,25-Dihydroxyvitamin D3/vitamin D receptor suppresses brown adipocyte differentiation and mitochondrial respiration

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• 作者：Carolyn J. Ricciardi ; Jiyoung Bae ; Debora Esposito…
• 关键词：Vitamin D receptor ; Brown adipocyte ; UCP1 ; Mitochondrial respiration
• 刊名：European Journal of Nutrition
• 出版年：2015
• 出版时间：September 2015
• 年：2015
• 卷：54
• 期：6
• 页码：1001-1012
• 全文大小：2,094 KB
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• 作者单位：Carolyn J. Ricciardi (1)
  Jiyoung Bae (1)
  Debora Esposito (3) (4)
  Slavko Komarnytsky (3) (4)
  Pan Hu (1)
  Jiangang Chen (1) (2)
  Ling Zhao (1)
  
  1. Department of Nutrition, University of Tennessee, 1215 W. Cumberland Ave, Knoxville, TN, 37996, USA
  3. North Carolina Research Campus, Plants for Human Health Institute, North Carolina State University, Kannapolis, NC, 28081, USA
  4. Department of Food, Bioprocessing, and Nutrition Sciences, North Carolina State University, Raleigh, NC, 27607, USA
  2. Department of Public Health, University of Tennessee, Knoxville, TN, 37996, USA
  
• 刊物类别：Chemistry and Materials Science
• 刊物主题：Chemistry
  Nutrition
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1436-6215

文摘

Purpose The vitamin D system plays a role in metabolism regulation. 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) suppressed 3T3-L1 white adipocyte differentiation. Vitamin D receptor (VDR) knockout mice showed increased energy expenditure, whereas mice with adipose-specific VDR over-expression showed decreased energy expenditure. Brown adipose tissue (BAT), now known to be present in adult humans, functions in non-shivering thermogenesis by uncoupling ATP synthesis from respiration and plays an important role in energy expenditure. However, the effects of 1,25(OH)2D3/VDR on brown adipocyte differentiation and mitochondrial respiration have not been reported. Methods mRNA expression of VDR and the metabolizing enzymes 1α-hydroxylase (CYP27B1) and 24-hydroxylase (CYP24A1) were examined in BAT of mice models of obesity and during brown adipocyte differentiation. The effects of 1,25(OH)2D3 and VDR over-expression on brown adipocyte differentiation and functional outcomes were evaluated. Results No significant changes in mRNA of VDR and CYP27B1 were noted in both diet-induced obese (DIO) and ob/ob mice, whereas uncoupling protein 1 mRNA was downregulated in BAT of ob/ob, but not DIO mice when compared to the controls. In contrast, mRNA of VDR, CYP24A1, and CYP27B1 were downregulated during brown adipocyte differentiation in vitro. 1,25(OH)2D3 dose-dependently suppressed brown adipocyte differentiation, accompanied by suppressed isoproterenol-stimulated oxygen consumption rates (OCR), maximal OCR and OCR from proton leak. Consistently, over-expression of VDR also suppressed brown adipocyte differentiation. Further, both 1,25(OH)2D3 and VDR over-expression suppressed PPARγ transactivation in brown preadipocytes. Conclusion Our results demonstrate the suppressive effects of 1,25(OH)2D3/VDR signaling on brown adipocyte differentiation and mitochondrial respiration. The role of 1,25(OH)2D3/VDR system in regulating BAT development and function in obesity warrant further investigation.