Roles for Prlhr/GPR10 and Npffr2/GPR74 in feeding responses to PrRP
Objective: Several groups of neurons in the NTS suppress food intake, including Prlh-expressing neurons (NTSPrlh cells). Not only does the artificial activation of NTSPrlh cells decrease feeding, but also the expression of Prlh (which encodes the neuropeptide PrRP) and neurotransmission by NTSPrlh n...
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Elsevier
2025-02-01
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| Series: | Molecular Metabolism |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2212877824002242 |
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| author | Yi Wang Weiwei Qiu Stace Kernodle Carly Parker Marc-Antonio Padilla Jiaao Su Abigail J. Tomlinson Stephanie Oldham Joss Field Elise Bernard David Hornigold Christopher J. Rhodes David P. Olson Randy J. Seeley Martin G. Myers, Jr |
| author_facet | Yi Wang Weiwei Qiu Stace Kernodle Carly Parker Marc-Antonio Padilla Jiaao Su Abigail J. Tomlinson Stephanie Oldham Joss Field Elise Bernard David Hornigold Christopher J. Rhodes David P. Olson Randy J. Seeley Martin G. Myers, Jr |
| author_sort | Yi Wang |
| collection | DOAJ |
| description | Objective: Several groups of neurons in the NTS suppress food intake, including Prlh-expressing neurons (NTSPrlh cells). Not only does the artificial activation of NTSPrlh cells decrease feeding, but also the expression of Prlh (which encodes the neuropeptide PrRP) and neurotransmission by NTSPrlh neurons contributes to the restraint of food intake and body weight, especially in animals fed a high fat diet (HFD). We set out to determine roles for putative PrRP receptors in the response to NTS PrRP and exogenous PrRP-related peptides. Methods: We used animals lacking PrRP receptors GPR10 and/or GPR74 (encoded by Prlhr and Npffr2, respectively) to determine roles for each in the restraint of food intake and body weight by the increased expression of Prlh in NTSPrlh neurons (NTSPrlhOX mice) and in response to the anorectic PrRP analog, p52. Results: Although Prlhr played a crucial role in the restraint of food intake and body weight in HFD-fed control animals, the combined absence of Prlhr and Npffr2 was required to abrogate the restraint of food intake in NTSPrlhOX mice. p52 suppressed feeding independently of both receptors, however. Conclusions: Hence, each receptor can participate in the NTSPrlh-mediated suppression of food intake and body weight gain, while PrRP analog treatment can mediate its effects via distinct systems. While Prlhr plays a crucial role in the physiologic restraint of weight gain, the action of either receptor is capable of ameliorating obesity in response to enhanced NTSPrlh signaling. |
| format | Article |
| id | doaj-art-a62d717967f54c529f7868b688424c5e |
| institution | Kabale University |
| issn | 2212-8778 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Molecular Metabolism |
| spelling | doaj-art-a62d717967f54c529f7868b688424c5e2025-02-01T04:11:58ZengElsevierMolecular Metabolism2212-87782025-02-0192102093Roles for Prlhr/GPR10 and Npffr2/GPR74 in feeding responses to PrRPYi Wang0Weiwei Qiu1Stace Kernodle2Carly Parker3Marc-Antonio Padilla4Jiaao Su5Abigail J. Tomlinson6Stephanie Oldham7Joss Field8Elise Bernard9David Hornigold10Christopher J. Rhodes11David P. Olson12Randy J. Seeley13Martin G. Myers, Jr14Department 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, ChinaDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USADepartment of Surgery, University of Michigan, Ann Arbor, MI, USADepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USADepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USADepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USADepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USAEarly Cardiovascular Renal and Metabolism, BioPharmaceuticals, R&D, AstraZeneca, Cambridge, UKEarly Cardiovascular Renal and Metabolism, BioPharmaceuticals, R&D, AstraZeneca, Cambridge, UKHit Discovery, Discovery Sciences, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UKEarly Cardiovascular Renal and Metabolism, BioPharmaceuticals, R&D, AstraZeneca, Cambridge, UKEarly Cardiovascular Renal and Metabolism, BioPharmaceuticals, R&D, AstraZeneca, Cambridge, UKDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA; Department of Pediatrics, University of Michigan, Ann Arbor, MI, USADepartment of Surgery, University of Michigan, Ann Arbor, MI, USA; Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USADepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA; Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA; Corresponding author. Department of Internal Medicine, Division of Metabolism, Endocrinology and Diabetes, University of Michigan Medical School, 2700 Plymouth Rd., Bldg 20, Room 2822, Ann Arbor, MI 48109, USA.Objective: Several groups of neurons in the NTS suppress food intake, including Prlh-expressing neurons (NTSPrlh cells). Not only does the artificial activation of NTSPrlh cells decrease feeding, but also the expression of Prlh (which encodes the neuropeptide PrRP) and neurotransmission by NTSPrlh neurons contributes to the restraint of food intake and body weight, especially in animals fed a high fat diet (HFD). We set out to determine roles for putative PrRP receptors in the response to NTS PrRP and exogenous PrRP-related peptides. Methods: We used animals lacking PrRP receptors GPR10 and/or GPR74 (encoded by Prlhr and Npffr2, respectively) to determine roles for each in the restraint of food intake and body weight by the increased expression of Prlh in NTSPrlh neurons (NTSPrlhOX mice) and in response to the anorectic PrRP analog, p52. Results: Although Prlhr played a crucial role in the restraint of food intake and body weight in HFD-fed control animals, the combined absence of Prlhr and Npffr2 was required to abrogate the restraint of food intake in NTSPrlhOX mice. p52 suppressed feeding independently of both receptors, however. Conclusions: Hence, each receptor can participate in the NTSPrlh-mediated suppression of food intake and body weight gain, while PrRP analog treatment can mediate its effects via distinct systems. While Prlhr plays a crucial role in the physiologic restraint of weight gain, the action of either receptor is capable of ameliorating obesity in response to enhanced NTSPrlh signaling.http://www.sciencedirect.com/science/article/pii/S2212877824002242NTSFood intakeObesityPrlhPrlhrNpffr2 |
| spellingShingle | Yi Wang Weiwei Qiu Stace Kernodle Carly Parker Marc-Antonio Padilla Jiaao Su Abigail J. Tomlinson Stephanie Oldham Joss Field Elise Bernard David Hornigold Christopher J. Rhodes David P. Olson Randy J. Seeley Martin G. Myers, Jr Roles for Prlhr/GPR10 and Npffr2/GPR74 in feeding responses to PrRP Molecular Metabolism NTS Food intake Obesity Prlh Prlhr Npffr2 |
| title | Roles for Prlhr/GPR10 and Npffr2/GPR74 in feeding responses to PrRP |
| title_full | Roles for Prlhr/GPR10 and Npffr2/GPR74 in feeding responses to PrRP |
| title_fullStr | Roles for Prlhr/GPR10 and Npffr2/GPR74 in feeding responses to PrRP |
| title_full_unstemmed | Roles for Prlhr/GPR10 and Npffr2/GPR74 in feeding responses to PrRP |
| title_short | Roles for Prlhr/GPR10 and Npffr2/GPR74 in feeding responses to PrRP |
| title_sort | roles for prlhr gpr10 and npffr2 gpr74 in feeding responses to prrp |
| topic | NTS Food intake Obesity Prlh Prlhr Npffr2 |
| url | http://www.sciencedirect.com/science/article/pii/S2212877824002242 |
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