Evidence mapPaperPMID 41508705Full record

ArticleDiabetes, obesity & metabolism2026

GLP-1R biased cAMP agonism maintains glycemic control with reduced malaise and emesis in preclinical mammalian models.

Caitlin Baumer-Harrison, Danya Aldaghma, Alex D White, Sarah V Applebey, Allison M Pataro, Allaha Z Mohiby, Brandon Alonso, Allison G Xiao, Libbey S O'Farrell, Yuewei Qian and 9 more

Abstract read
In one paragraph

Article in Diabetes, obesity & metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors.

Caitlin Baumer-HarrisonDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.ORCID 0000-0002-6287-5887
Danya AldaghmaDepartment of Biobehavioral Health Sciences, School of Nursing, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Alex D WhiteDivision of Diabetes and Complications, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, Indiana, USA.
Sarah V ApplebeyDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Allison M PataroDepartment of Biological Sciences, University of Southern California, Los Angeles, California, USA.
Allaha Z MohibyDepartment of Biobehavioral Health Sciences, School of Nursing, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Brandon AlonsoDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Allison G XiaoDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Libbey S O'FarrellDivision of Diabetes and Complications, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, Indiana, USA.
Yuewei QianDivision of Diabetes and Complications, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, Indiana, USA.
Tamer CoskunDivision of Diabetes and Complications, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, Indiana, USA.ORCID 0000-0002-2481-133X
Matthew P CoghlanDivision of Diabetes and Complications, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, Indiana, USA.
Francis S WillardDivision of Diabetes and Complications, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, Indiana, USA.
Minrong AiDivision of Diabetes and Complications, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, Indiana, USA.
Kyle W SloopDivision of Diabetes and Complications, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, Indiana, USA.
Robert P DoyleDepartment of Chemistry, Syracuse University, Syracuse, New York, USA.
Tito BornerDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Bart C De JongheDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.ORCID 0000-0002-6980-5355
Matthew R HayesDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.ORCID 0000-0001-9782-6551

Funding

Neural Mechanisms of Nausea, Vomiting, and Energy DysregulationR01DK112812 · UNIVERSITY OF PENNSYLVANIA · 2025 to 2025
$640k
Diabetes Research Center, Institute for Diabetes, Obesity and Metabolism, Perelman School of Medicine, University of Pennsylvania DK112812NIDDK NIH HHS R01 DK112812
6 · The paper itself

Abstract

aimsGlucagon-like peptide-1 receptor (GLP-1R) agonists improve glycemic control and promote weight loss in diabetes and obesity but are also associated with gastrointestinal adverse events, including nausea and emesis in many patients. These concerns highlight the need for the development of novel GLP-1R agonists that minimize these side effects while maintaining beneficial metabolic outcomes. Here, we investigate the in vivo effects of exendin-4-Phe1 (Ex-Phe1), a GLP-1R biased agonist. MATERIALS AND

methodsIn three pre-clinical species, mice (n = 43), rats (n = 54), and musk shrews (n = 30), we examined in vivo glycemic control, feeding, and nausea/emesis following native Ex-4 and Ex-Phe1 administration. We also used cFos expression following Ex-4 and Ex-Phe1 administration to examine neural activation in regions involved in mediating nausea and emetic side effects of GLP-1R agonism.

resultsIn vitro studies show Ex-Phe1 favors cAMP signaling with reduced β-arrestin recruitment. Compared to Ex-4, Ex-Phe1 produced fewer emetic episodes in musk shrews (Suncus murinus) and little to no pica, a proxy for nausea, in rats. Ex-Phe1 effects on food intake and body weight varied by species, while Ex-4 and Ex-Phe1 similarly enhanced glucose tolerance in all species. Ex-4 and Ex-Phe1 increased cFos expression within brain regions linked to nausea and emesis in all species.

conclusionsCollectively, Ex-Phe1 maintains glycemic benefits in all three species, but putatively blunts the ability of the CNS GLP-1R+ cells to drive anorexia and weight loss, as well as unwanted adverse events (nausea/emesis) in rats and musk shrews.

Indexed as

Cyclic AMPGlucagon-Like Peptide-1 Receptor AgonistsGlycemic ControlHypoglycemic AgentsNauseaPeptidesVomitingAnimalsBlood GlucoseEatingExenatideGlucagon-Like Peptide-1 ReceptorMaleMiceRatsRats, Sprague-DawleyBlood GlucoseCyclic AMPExenatideGlp1r protein, ratGlucagon-Like Peptide-1 ReceptorGlucagon-Like Peptide-1 Receptor AgonistsHypoglycemic AgentsPeptidesVenomsbiased agonistemesisexendin‐4GLP‐1Rmalaisenauseaβ‐arrestin

Identifiers

PMID41508705
PMCPMC12981003

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.