Evidence map›Paper›PMID 28792489›Full record

ArticleInternational journal of obesity (2005)2017

l-phenylalanine modulates gut hormone release and glucose tolerance, and suppresses food intake through the calcium-sensing receptor in rodents.

A Alamshah, E Spreckley, M Norton, J S Kinsey-Jones, A Amin, A Ramgulam, Y Cao, R Johnson, K Saleh, E Akalestou and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in International journal of obesity (2005), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.8field-weighted citation impact, top 4% of its field
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

56 citing papers in PubMed, 126 citations in OpenAlex.

  1. Effects of physical form ofThe British journal of nutrition · 2024
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  16. Nutrient Combinations Sensed by L-Cell Receptors Potentiate GLP-1 Secretion.International journal of molecular sciences · 2024
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  19. The Synergism of HumanJournal of microbiology and biotechnology · 2023
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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 at 3 institutions in 1 country.

A AlamshahSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
E SpreckleySection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
M NortonSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
J S Kinsey-JonesSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
A AminSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
A RamgulamSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
Y CaoSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
R JohnsonSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
K SalehSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
E AkalestouSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
Z MalikSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
N Gonzalez-AbuinSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
A JomardSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
R AmarsiSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
A MoollaSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
P R SargentTasteTech Ltd, Bristol, UK.
G W GrayTasteTech Ltd, Bristol, UK.
S R BloomSection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
K G MurphySection of Endocrinology and Investigative Medicine, Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
Hammersmith Hospital · GBImperial College London · GBUniversity of Oxford · GB

Funding

Biotechnology and Biological Sciences Research Council BB/I001816/1Medical Research Council MR/J010944/1National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/K500379/1
6 · The paper itself

Abstract

objectiveHigh-protein diets (HPDs) are associated with greater satiety and weight loss than diets rich in other macronutrients. The exact mechanisms by which HPDs exert their effects are unclear. However, evidence suggests that the sensing of amino acids produced as a result of protein digestion may have a role in appetite regulation and satiety. We investigated the effects of l-phenylalanine (L-Phe) on food intake and glucose homeostasis in rodents.

methodsWe investigated the effects of the aromatic amino-acid and calcium-sensing receptor (CaSR) agonist l-phenylalanine (L-Phe) on food intake and the release of the gastrointestinal (GI) hormones peptide YY (PYY), glucagon-like peptide-1 (GLP-1) and ghrelin in rodents, and the role of the CaSR in mediating these effects in vitro and in vivo. We also examined the effect of oral l-Phe administration on glucose tolerance in rats.

resultsOral administration of l-Phe acutely reduced food intake in rats and mice, and chronically reduced food intake and body weight in diet-induced obese mice. Ileal l-Phe also reduced food intake in rats. l-Phe stimulated GLP-1 and PYY release, and reduced plasma ghrelin, and also stimulated insulin release and improved glucose tolerance in rats. Pharmacological blockade of the CaSR attenuated the anorectic effect of intra-ileal l-Phe in rats, and l-Phe-induced GLP-1 release from STC-1 and primary L cells was attenuated by CaSR blockade.

conclusionsl-Phe reduced food intake, stimulated GLP-1 and PYY release, and reduced plasma ghrelin in rodents. Our data provide evidence that the anorectic effects of l-Phe are mediated via the CaSR, and suggest that l-Phe and the CaSR system in the GI tract may have therapeutic utility in the treatment of obesity and diabetes. Further work is required to determine the physiological role of the CaSR in protein sensing in the gut, and the role of this system in humans.

Indexed as

Glucose IntoleranceAnimalsAppetite DepressantsAppetite RegulationDisease Models, AnimalEatingEnergy MetabolismGastrointestinal HormonesMaleMiceMice, Inbred C57BLPhenylalanineRatsRats, WistarReceptors, Calcium-SensingReceptors, Gastrointestinal HormoneAppetite DepressantsGastrointestinal HormonesPhenylalanineReceptors, Calcium-SensingReceptors, Gastrointestinal Hormone

Identifiers

PMID28792489
PMCPMC5678004
OpenAlexW2744602602

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.