Amylin: Pharmacology, Physiology, and Clinical Potential
Open accessAbstract
Amylin is a pancreatic β-cell hormone that produces effects in several different organ systems. Here, we review the literature in rodents and in humans on amylin research since its discovery as a hormone about 25 years ago. Amylin is a 37-amino-acid peptide that activates its specific receptors, which are multisubunit G protein-coupled receptors resulting from the coexpression of a core receptor protein with receptor activity-modifying proteins, resulting in multiple receptor subtypes. Amylin's major role is as a glucoregulatory hormone, and it is an important regulator of energy metabolism in health and disease. Other amylin actions have also been reported, such as on the cardiovascular system or on bone. Amylin acts principally in the circumventricular organs of the central nervous system and functionally interacts with other metabolically active hormones such as cholecystokinin, leptin, and estradiol. The amylin-based peptide, pramlintide, is used clinically to treat type 1 and type 2 diabetes. Clinical studies in obesity have shown that amylin agonists could also be useful for weight loss, especially in combination with other agents.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Amylin acts on amylin receptors in the brainstem to reduce food intake and improves glucose metabolism by delaying gastric emptying and inhibiting glucagon secretion.
“Amylin acts on amylin receptors in the brainstem to reduce food intake [83] and improves glucose metabolism by delaying gastric emptying and inhibiting glucagon secretion [84, 85].”
From What is the pipeline for future medications for obesity? (2025) · cites this paper as [85]
Amylin increases satiety and reduces food intake through actions on the area postrema at the brainstem.
“Amylin also increases satiety and reduces food intake through actions on the area postrema at the brainstem, and the reduction in food intake is not accompanied by the expected decrease in energy expenditure [61].”
The reduction in food intake with amylin is not accompanied by the expected decrease in energy expenditure.
“Amylin also increases satiety and reduces food intake through actions on the area postrema at the brainstem, and the reduction in food intake is not accompanied by the expected decrease in energy expenditure [61].”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 308 · Cited by 400
- Authors
- Hay, D. L., Chen, S., Lutz, T. A., Parkes, D. G., & Roth, J. D.
- Affiliations
- University of Auckland (NZ)
- Venue
- Pharmacological Reviews
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 67
- Issue
- 3
- Pages
- 564-600
- ISSN
- 0031-6997 (ISSN-L)
- OpenAlex
- W2157652680
- Cited by
- 400
- References
- 308
- Citations by year
- 2026: 37 · 2025: 54 · 2024: 42 · 2023: 30 · 2022: 34 · 2021: 44 · 2020: 42 · 2019: 30 · 2018: 31 · 2017: 32 · 2016: 19 · 2015: 5
- FWCI
- 3.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Pharmacological Reviews (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- amylin, G protein-coupled receptors, receptor activity-modifying proteins, glucoregulation, energy metabolism, cardiovascular effects, bone metabolism, circumventricular organs, cholecystokinin, leptin, estradiol, pramlintide, type 1 diabetes, type 2 diabetes, obesity, weight loss
- MeSH terms
- Animals, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Energy Metabolism, Humans, Hypoglycemic Agents, Weight Loss, Islet Amyloid Polypeptide
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
