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The Journal of Neuroscience, June 28, 2006, 26(26):7116-7120; doi:10.1523/JNEUROSCI.0672-06.2006

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Brief Communications
Adenoviral-Mediated Modulation of Sim1 Expression in the Paraventricular Nucleus Affects Food Intake

Chun Yang,¹ David Gagnon,^2,3 Pascal Vachon,⁴ André Tremblay,¹ Emile Levy,¹ Bernard Massie,^2,3 and Jacques L. Michaud¹

¹Centre de Recherche, Hôpital Sainte-Justine, Montréal, Québec, Canada H3T 1C5, ²Institut de Recherche en Biotechnologie, Conseil National de Recherche du Canada, Montréal, Québec, Canada H4P 2R2, ³Département de Microbiologie et Immunologie, Faculté de Médecine, Université de Montréal, Montréal, Québec, Canada H3C 3T4, and ⁴Faculté de Médecine Vétérinaire, Université de Montréal, Saint-Hyacinthe, Québec, Canada J2S 7C6

Correspondence should be addressed to Dr. Jacques L. Michaud, Research Center, Hôpital Sainte-Justine, 3175 Côte Sainte-Catherine, Montréal, Québec, Canada H3T 1C5. Email: jacques.michaud{at}recherche-ste-justine.qc.ca

Haploinsufficency of Sim1, which codes for a basic helix-loop-helix–PAS (PER-ARNT-SIM) transcription factor, causes hyperphagia in mice and humans, without decrease in energy expenditure. Sim1 is expressed in several areas of the brain, including the developing and postnatal paraventricular nucleus (PVN), a region of the hypothalamus that controls food intake. We have previously found that the number of PVN cells is decreased in Sim1^+/– mice, suggesting that their hyperphagia is caused by a developmental mechanism. However, the possibility that Sim1 functions in the postnatal PVN to control food intake cannot be ruled out. To explore this hypothesis, we used adenoviral vectors to modulate Sim1 expression in the postnatal PVN of wild-type mice. Unilateral stereotaxic injection into the PVN of an adenoviral vector producing a short hairpin RNA directed against Sim1 resulted in a significant increase in food intake, which peaked to 22% 6 d after the procedure, compared with the injection of a control virus. In contrast, injection of an adenovirus that expresses Sim1 induced a decrease in food intake that was maximal on the seventh day after the procedure, reaching 20%. The impact of bilateral injections of these vectors into the PVN was not greater than that of unilateral injections. Together, these results strongly suggest that Sim1 functions along a physiological pathway to control food intake.

Key words: hypothalamus; mice; energy; transcription factor; development; obesity

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Received Feb. 15, 2006; revised May 22, 2006; accepted May 23, 2006.

Correspondence should be addressed to Dr. Jacques L. Michaud, Research Center, Hôpital Sainte-Justine, 3175 Côte Sainte-Catherine, Montréal, Québec, Canada H3T 1C5. Email: jacques.michaud{at}recherche-ste-justine.qc.ca

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