AI Article Synopsis
- The study identifies Ahi1 protein as a key player in regulating feeding behavior by interacting with the serotonin receptor 2C (5-HT(2C)R), which is crucial for appetite control.
- Ahi1 promotes the degradation of 5-HT(2C)R and shows altered expression during fasting; increased Ahi1 levels lead to decreased 5-HT(2C)R levels.
- Knockdown of Ahi1 results in increased 5-HT(2C)R expression and reduced food intake, indicating Ahi1’s role in modulating serotonin signaling associated with feeding behavior.*
Article Abstract
It is indicated that there are important molecules interacting with brain nervous systems to regulate feeding and energy balance by influencing the signaling pathways of these systems, but relatively few of the critical players have been identified. In the present study, we provide the evidence for the role of Abelson helper integration site 1 (Ahi1) protein as a mediator of feeding behavior through interaction with serotonin receptor 2C (5-HT(2C)R), known for its critical role in feeding and appetite control. First, we demonstrated the co-localization and interaction between hypothalamic Ahi1 and 5-HT(2C)R. Ahi1 promoted the degradation of 5-HT(2C)R through the lysosomal pathway. Then, we investigated the effects of fasting on the expression of hypothalamic Ahi1 and 5-HT(2C)R. Fasting resulted in an increased Ahi1 expression and a concomitant decreased expression of 5-HT(2C)R. Knockdown of hypothalamic Ahi1 led to a concomitant increased expression of 5-HT(2C)R and a decrease of food intake and body weight. Last, we found that Ahi1 could regulate the expression of neuropeptide Y and proopiomelanocortin. Taken together, our results indicate that Ahi1 mediates feeding behavior by interacting with 5-HT(2C)R to modulate the serotonin signaling pathway.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3265901 | PMC |
| http://dx.doi.org/10.1074/jbc.M111.277871 | DOI Listing |
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