ArticleDiabetes2022
GIPR Agonism Inhibits PYY-Induced Nausea-Like Behavior.
Article in Diabetes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 61 citations in OpenAlex.
- Clinical Potential of GIP in Type 2 Diabetes and Obesity.Diabetes care · 2026Review
- Distinct brain regions mediate regulation of food intake in response to GIPR agonism or antagonism.Nature metabolism · 2026Article
- Functional segregation of body-brain signals in the area postrema.bioRxiv : the preprint server for biology · 2026Article
- GIPR signaling modulates PYY-induced hypophagia and malaise in rodents.Molecular metabolism · 2026Article
- GIP receptor agonism suppresses inflammation-induced aversion and food intake via distinct circuits.Cell reports · 2026Article
- Tirzepatide for obesity without diabetes: mechanistic insights, clinical evidence, and future directions.Frontiers in pharmacology · 2026Review
- [A personalized, evidence-based approach to obesity therapy using clinical algorithms: semaglutide or tirzepatide].Problemy endokrinologii · 2025Article
- Sensory signals for nausea.Trends in neurosciences · 2025Review
- GIP receptor agonism suppresses inflammation-induced aversion and food intake via distinct circuits.bioRxiv : the preprint server for biology · 2025Article
- Review
- A Contemporary Rationale for Agonism of the GIP Receptor in the Treatment of Obesity.Diabetes · 2025Review
- Evolving incretin-based therapies in Japan: optimizing treatment strategies for diverse clinical and socioeconomical profiles in type 2 diabetes.Diabetology international · 2025Review
- Refractory Nausea and Vomiting Due to Central Nervous System Injury: A Focused Review.Life (Basel, Switzerland) · 2025Review
- Molecular Design of Unimolecular Tetra-Receptor Agonists.Journal of the American Chemical Society · 2025Article
- GIPR-Ab/GLP-1 peptide-antibody conjugate requires brain GIPR and GLP-1R for additive weight loss in obese mice.Nature metabolism · 2025Article
- The Premise of the Paradox: Examining the Evidence That Motivated GIPR Agonist and Antagonist Drug Development Programs.Journal of clinical medicine · 2025Review
- Investigating Mechanically Activated Currents from Trigeminal Neurons of Nonhuman Primates.eNeuro · 2025Article
- Focus on Glucagon-like Peptide-1 Target: Drugs Approved or Designed to Treat Obesity.International journal of molecular sciences · 2025Review
- Neural pathways of nausea and roles in energy balance.Current opinion in neurobiology · 2025Review
- The GIP receptor activates futile calcium cycling in white adipose tissue to increase energy expenditure and drive weight loss in mice.Cell metabolism · 2025Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The induction of nausea and emesis is a major barrier to maximizing the weight loss profile of obesity medications, and therefore, identifying mechanisms that improve tolerability could result in added therapeutic benefit. The development of peptide YY (PYY)-based approaches to treat obesity are no exception, as PYY receptor agonism is often accompanied by nausea and vomiting. Here, we sought to determine whether glucose-dependent insulinotropic polypeptide (GIP) receptor (GIPR) agonism reduces PYY-induced nausea-like behavior in mice. We found that central and peripheral administration of a GIPR agonist reduced conditioned taste avoidance (CTA) without affecting hypophagia mediated by a PYY analog. The receptors for GIP and PYY (Gipr and Npy2r) were found to be expressed by the same neurons in the area postrema (AP), a brainstem nucleus involved in detecting aversive stimuli. Peripheral administration of a GIPR agonist induced neuronal activation (cFos) in the AP. Further, whole-brain cFos analyses indicated that PYY-induced CTA was associated with augmented neuronal activity in the parabrachial nucleus (PBN), a brainstem nucleus that relays aversive/emetic signals to brain regions that control feeding behavior. Importantly, GIPR agonism reduced PYY-mediated neuronal activity in the PBN, providing a potential mechanistic explanation for how GIPR agonist treatment reduces PYY-induced nausea-like behavior. Together, the results of our study indicate a novel mechanism by which GIP-based therapeutics may have benefit in improving the tolerability of weight loss agents.
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