An analogue of the Prolactin Releasing Peptide reduces obesity and promotes adult neurogenesis
- PMID: 38177913
- PMCID: PMC10897398
- DOI: 10.1038/s44319-023-00016-2
An analogue of the Prolactin Releasing Peptide reduces obesity and promotes adult neurogenesis
Abstract
Hypothalamic Adult Neurogenesis (hAN) has been implicated in regulating energy homeostasis. Adult-generated neurons and adult Neural Stem Cells (aNSCs) in the hypothalamus control food intake and body weight. Conversely, diet-induced obesity (DIO) by high fat diets (HFD) exerts adverse influence on hAN. However, the effects of anti-obesity compounds on hAN are not known. To address this, we administered a lipidized analogue of an anti-obesity neuropeptide, Prolactin Releasing Peptide (PrRP), so-called LiPR, to mice. In the HFD context, LiPR rescued the survival of adult-born hypothalamic neurons and increased the number of aNSCs by reducing their activation. LiPR also rescued the reduction of immature hippocampal neurons and modulated calcium dynamics in iPSC-derived human neurons. In addition, some of these neurogenic effects were exerted by another anti-obesity compound, Liraglutide. These results show for the first time that anti-obesity neuropeptides influence adult neurogenesis and suggest that the neurogenic process can serve as a target of anti-obesity pharmacotherapy.
Keywords: Adult neurogenesis; Anti-obesity peptides; Hypothalamus; Neural stem cells; Prolactin Releasing Peptide.
© 2023. The Author(s).
Conflict of interest statement
The authors declare no competing interests.
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