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Physiol. Genomics 31: 306-314, 2007. First published August 7, 2007; doi:10.1152/physiolgenomics.00110.2007
1094-8341/07 $8.00
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Received 14 May 2007; accepted in final form 31 July 2007.
Physiological Genomics 31:306-314 (2007)
1094-8341/07 $8.00 © 2007 American Physiological Society

Transcript of protein kinase A knock-down modulates feeding behavior and neuropeptide Y gene expression in phenylpropanolamine-treated rats

Yih-Shou Hsieh 1, Shun-Fa Yang 2, Shu-Chen Chu 4 and Dong-Yih Kuo 3

1 Institute of Biochemistry, Central Taiwan University of Science and Technology, Taichung City, Taiwan, Republic of China
2 Institute of Medicine, Central Taiwan University of Science and Technology, Taichung City, Taiwan, Republic of China
3 Department of Physiology, Chung Shan Medical University, Central Taiwan University of Science and Technology, Taichung City, Taiwan, Republic of China
Department of Food Science, Central Taiwan University of Science and Technology, Taichung City, Taiwan, Republic of China

Neuropeptide Y (NPY) is an appetite-controlling neuromodulator that contributes to the appetite-suppressing effect of phenylpropanolamine (PPA). Aims of this study were to investigate whether protein kinase A (PKA) signaling is involved in regulating NPY gene expression and PPA-induced anorexia. Rats were given daily with PPA for 5 days. Changes in daily food intake and hypothalamic NPY, PKA, cAMP response element binding protein (CREB), and pro-opiomelanocortin (POMC) gene expression were measured and compared. To further determine if PKA was involved, intracerebroventricular infusions of antisense oligodeoxynucleotide were performed at 60 min before daily PPA treatment in freely moving rats. Results showed that daily PKA, CREB, and POMC expression were increased following PPA treatment, which showed a closely reverse relationship with alterations of decreased feeding behaviors and NPY mRNA levels. Results also showed that PKA knock-down could block PPA-induced anorexia as well as restore NPY mRNA level, indicating the involvement of PKA signaling in the regulation of NPY gene expression. It is suggested that hypothalamic PKA signaling may participate in the central regulation of PPA-mediated appetite suppression via the modulation of hypothalamic NPY gene expression. The present findings reveal that manipulations at the molecular level of PKA or cAMP may allow the development of therapeutic agents to improve the undesirable properties of PPA or other amphetamine-like anorectic drugs.

anorectic agent; antisense oligonucleotide; signal transduction; hypothalamus; appetite






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