ArticleEndocrinology2008
Caudal brainstem processing is sufficient for behavioral, sympathetic, and parasympathetic responses driven by peripheral and hindbrain glucagon-like-peptide-1 receptor stimulation.
Article in Endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers.
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.
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.
Who cites it
146 citing papers in PubMed, 211 citations in OpenAlex.
- Glucagon-Like Peptide-1 Signaling in Learning and Memory: Evidence, Mechanisms, and Therapeutic Implications.Biological psychiatry · 2026Review
- The central amygdala gates exogenous glucagon-like peptide 1 signals.Molecular metabolism · 2026Article
- Semaglutide, tirzepatide, and retatrutide attenuate the interoceptive effects of alcohol in male and female rats.Psychopharmacology · 2026Article
- GLP-1 at the Metabolic-Cognitive Interface: Reward, Affect, and Memory.Comprehensive physiology · 2026Review
- GLP-1R biased cAMP agonism maintains glycemic control with reduced malaise and emesis in preclinical mammalian models.Diabetes, obesity & metabolism · 2026Article
- Incretin-Based Therapies: A Novel Pathway in Addiction Treatment.Journal of clinical medicine · 2026Review
- The estrous cycle moderates the food and body weight suppressive effects of glucagon-like peptide-1 receptor agonism.Diabetes, obesity & metabolism · 2026Article
- Advantage of Semaglutide: Comprehensive Analysis of Metabolic Impact of Semaglutide-Treated and Pair-Fed Rats.Comprehensive physiology · 2025Article
- Mechanisms of glucagon-like-peptide 1 in the brain beyond metabolic effects.Annals of pediatric endocrinology & metabolism · 2025Article
- Pharmacological and physiological activation of TGR5 in the NTS lowers food intake by enhancing leptin-STAT3 signaling.Nature communications · 2025Article
- Article
- Glucagon-like peptide-1 receptor modulates cerebrospinal fluid secretion and intracranial pressure in rats.Fluids and barriers of the CNS · 2025Article
- Vagal Sensory Gut-Brain Pathways That Control Eating-Satiety and Beyond.Comprehensive physiology · 2025Review
- The Chimeric Peptide (GEP44) Reduces Body Weight and Both Energy Intake and Energy Expenditure in Diet-Induced Obese Rats.International journal of molecular sciences · 2025Article
- Glucagon-Like Peptide-1 Links Ingestion, Homeostasis, and the Heart.Comprehensive Physiology · 2025Review
- GLP-1 and Its Analogs: Does Sex Matter?Endocrinology · 2025Review
- GLP-1 receptor agonist exenatide uncouples food intake from hedonic and anticipatory regulation in non-human primates: insights from an operant meal schedule paradigm.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- GLP-1R-positive neurons in the lateral septum mediate the anorectic and weight-lowering effects of liraglutide in mice.The Journal of clinical investigation · 2024Article
- Article
- Regulation of Energy and Glucose Homeostasis by the Nucleus of the Solitary Tract and the Area Postrema.Endocrinology and metabolism (Seoul, Korea) · 2024Review
86 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The effects of peripheral glucagon like peptide-1 receptor (GLP-1R) stimulation on feeding, gastric emptying, and energetic responses involve vagal transmission and central nervous system processing. Despite a lack of studies aimed at determining which central nervous system regions are critical for the GLP-1R response production, hypothalamic/forebrain processing is regarded as essential for these effects. Here the contribution of the caudal brainstem to the control of food intake, core temperature, heart rate, and gastric emptying responses generated by peripheral delivery of the GLP-1R agonist, exendin-4 (Ex-4), was assessed by comparing responses of chronic supracollicular decerebrate (CD) rats to those of pair-fed intact control rats. Responses driven by hindbrain intracerebroventricular (fourth i.c.v) delivery of Ex-4 were also evaluated. Intraperitoneal Ex-4 (1.2 and 3.0 microg/kg) suppressed glucose intake in both CD rats (5.0+/-1.2 and 4.4+/-1.1 ml ingested) and controls (9.4+/-1.5 and 7.7+/-0.8 ml ingested), compared with intakes after vehicle injections (13.1+/-2.5 and 13.2+/-1.7 ml ingested, respectively). Hindbrain ventricular Ex-4 (0.3 microg) also suppressed food intake in CD rats (4.7+/-0.6 ml ingested) and controls (11.0+/-2.9 ml ingested), compared with vehicle intakes (9.3+/-2.1 and 19.3+/-4.3 ml ingested, respectively). Intraperitoneal Ex-4 (0.12, 1.2, 2.4 microg/kg) reduced gastric emptying rates in a dose-related manner similarly for both CD and control rats. Hypothermia followed ip and fourth i.c.v Ex-4 in awake, behaving controls (0.6 and 1.0 C average suppression) and CD rats (1.5 and 2.5 C average suppression). Intraperitoneal Ex-4 triggered tachycardia in both control and CD rats. Results demonstrate that caudal brainstem processing is sufficient for mediating the suppression of intake, core temperature, and gastric emptying rates as well as tachycardia triggered by peripheral GLP-1R activation and also hindbrain-delivered ligand. Contrary to the literature, hypothalamic/forebrain processing and forebrain-caudal brainstem communication is not required for the observed responses.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.