Evidence map›Paper›PMID 27156041›Full record

ReviewTrends in endocrinology and metabolism: TEM2016

Metabolic Actions of the Type 1 Cholecystokinin Receptor: Its Potential as a Therapeutic Target.

Laurence J Miller, Aditya J Desai

Abstract readReview
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. GPCR drug discovery: new agents, targets and indications.Nature reviews. Drug discovery · 2025
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  20. Modulation of receptor signaling by metabolic environment.The American journal of clinical nutrition · 2017
    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

2 authors at 1 institution in 1 country.

Laurence J MillerDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Scottsdale, AZ, 85259, USA. Electronic address: miller@mayo.edu.
Aditya J DesaiDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Scottsdale, AZ, 85259, USA.
Mayo Clinic in Arizona · US

Funding

Type A CCK Receptor Structure, Function & RegulationR01DK032878 · NIDDK · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI MILLER, LAURENCE J · 1986 to 2014
$2.5M
NIDDK NIH HHS R01 DK032878
6 · The paper itself

Abstract

Cholecystokinin (CCK) regulates appetite and reduces food intake by activating the type 1 CCK receptor (CCK1R). Attempts to develop CCK1R agonists for obesity have yielded active agents that have not reached clinical practice. Here we discuss why, along with new strategies to target CCK1R more effectively. We examine signaling events and the possibility of developing agents that exhibit ligand-directed bias, to dissociate satiety activity from undesirable side effects. Potential allosteric sites of modulation are also discussed, along with desired properties of a positive allosteric modulator (PAM) without intrinsic agonist action as another strategy to treat obesity. These new types of CCK1R-active drugs could be useful as standalone agents or as part of a rational drug combination for management of obesity.

Indexed as

Allosteric RegulationAnimalsCholecystokininHumansObesityReceptor, Cholecystokinin AReceptors, CholecystokininCholecystokininReceptor, Cholecystokinin AReceptors, Cholecystokininbiased agonistscholecystokininpositive allosteric modulatorssatietytype 1 cholecystokinin receptor

Identifiers

PMID27156041
PMCPMC4992613
OpenAlexW2346041814

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.