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Effects of α-(prazosin and yohimbine) and β-receptors activity on cAMP generation and UCP1 gene expression in brown adipocytes

  • Hirendra M. Biswas EMAIL logo
Published/Copyright: April 18, 2018

Abstract

Background

Brown adipose tissue (BAT) contains both α- and β-adrenergic receptors. In the literature, the activity of α-adrenoreceptors is less documented, and their functions still remain puzzling. The present investigation has been undertaken to understand α-adrenoreceptors’ activity and their relation between uncoupling protein 1 (UCP1) mRNA expression and cyclic AMP (cAMP) generation in BAT.

Methods

BAT precursor cells from young mice were grown in culture. Cells were exposed to norepinephrine (NE) and other agents. RNA was isolated after harvesting the cells, and northern blot was performed. Filters were exposed to film after hybridization with nick-translated complementary DNA probes, and results were evaluated by scanning. Amersham assay kit was used for cAMP measurement.

Results

Treatment of prazosin and yohimbine separately with 1 μM of NE shows stimulation of UCP1 mRNA expression 106% and 154%, respectively, whereas with that of both drugs shows only 76%. cAMP generation occurs 282% with prazosin, 100% with yohimbine, and 382% with both drugs with 1 μM of NE, whereas it is 310%, 40%, and 358%, respectively, with 10 μM of NE.

Conclusions

Stimulation of thermogenesis after treatment of prazosin and NE may be due to the inhibition of phosphodiesterase enzyme and with yohimbine and NE indicates the possibility of inhibition of the inhibitory effect of α2- and stimulation of α1-receptors. Increase of cAMP concentration with yohimbine and both drugs with NE are not correlated to UCP1 mRNA expression. This indicates that the relationship between cAMP elevation and stimulation of thermogenesis is not simple. This study clearly shows the interaction between β- and α-adrenoreceptor activities.

Acknowledgments

The author is grateful to Prof. Barbara Cannon and Prof. Jan Nedregaard of the Department of Metabolic Research, Wenner-Gren Institute, Stockholm University, S-100 91 Stockholm, Sweden, for laboratory facilities, help, and valuable suggestions in performing this work. The author is extending his thanks to Dr. Chanda Karki, Principal, Kathmandu Medical College, Kathmandu, Nepal, for her interest on the research activities in the college. The author also acknowledges Mr. Umesh Bhattarai, Lecturer, Department of Physiology, Kathmandu Medical College, Kathmandu, Nepal, for his help in computer works.

  1. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  2. Research funding: Swedish Natural Science Research Council.

  3. Employment or leadership: None declared.

  4. Honorarium: None declared.

  5. Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

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Received: 2017-05-23
Accepted: 2018-01-15
Published Online: 2018-04-18
Published in Print: 2018-09-25

©2018 Walter de Gruyter GmbH, Berlin/Boston

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