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Roles for Prlhr/GPR10 and Npffr2/GPR74 in feeding responses to PrRP
Yi Wang1, Weiwei Qiu2, Stace Kernodle3
1Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA; Department of Metabolism and Endocrinology, National Clinical Research Center for Metabolic Diseases, the Second Xiangya Hospital, Central South University, Changsha, 410000, China.
Molecular Metabolism
|January 4, 2025
Summary
The study found that blocking both PrRP receptors (Prlhr and Npffr2) was necessary to eliminate the appetite-suppressing effects of NTSPrlh neuron activation. However, PrRP analog p52 reduced feeding independently of these receptors.
Area of Science:
- Neuroscience
- Endocrinology
- Obesity Research
Background:
- Neurons in the NTS (nucleus of the solitary tract) regulate food intake.
- Prolactin-releasing hormone (Prlh)-expressing neurons (NTSPrlh) in the NTS suppress feeding and body weight, particularly on a high-fat diet (HFD).
- Prlh encodes the neuropeptide PrRP, and its signaling is implicated in appetite control.
Purpose of the Study:
- To investigate the roles of PrRP receptors GPR10 (Prlhr) and GPR74 (Npffr2) in mediating the effects of NTSPrlh neuron signaling on food intake and body weight.
- To determine if the anorectic effects of the PrRP analog p52 are dependent on Prlhr and Npffr2.
Main Methods:
- Utilized genetically modified mice lacking PrRP receptors GPR10 (Prlhr) and/or GPR74 (Npffr2).
- Examined the effects of enhanced Prlh expression in NTSPrlh neurons (NTSPrlhOX mice) on food intake and body weight in these receptor-deficient mice.
- Administered the PrRP analog p52 to assess its effects on feeding independently of the studied receptors.
Main Results:
- Prlhr was crucial for restraining food intake and body weight in HFD-fed control mice.
- The combined absence of Prlhr and Npffr2 was required to abolish the food intake restraint observed in NTSPrlhOX mice.
- The PrRP analog p52 suppressed feeding independently of both Prlhr and Npffr2.
Conclusions:
- Both Prlhr and Npffr2 can contribute to NTSPrlh-mediated suppression of food intake and body weight.
- PrRP analog p52 exerts its anorectic effects through systems distinct from Prlhr and Npffr2.
- While Prlhr is vital for physiological weight gain restraint, either receptor can help mitigate obesity when NTSPrlh signaling is enhanced.
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