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Physiol. Genomics (August 7, 2007). doi:10.1152/physiolgenomics.00110.2007
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Submitted on May 14, 2007
Accepted on July 31, 2007

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

Yih-Shou Hsieh1, Shun-Fa Yang2, and Dong-Yih Kuo3*

1 Biochemistry, Chung Shan Medical University, Taiwan - Republic of China
2 Institute of Medicine, Chung Shan Medical University, Taiwan - Republic of China
3 Physiology, Chung Shan Medical University, Taiwan - Republic of China

* To whom correspondence should be addressed. E-mail: dykuo{at}csmu.edu.tw.

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 if protein kinase A (PKA) signaling was 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, c-AMP 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 c-AMP may allow the development of therapeutic agents to improve the undesirable properties of PPA or other amphetamine-like anorectic drugs.






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