Publication:
Can GLP-1 be a target for reward system related disorders? a qualitative synthesis and systematic review analysis of studies on palatable food, drugs of abuse, and alcohol

dc.contributor.coauthorDoğruöz, Ramazan Efe
dc.contributor.departmentKUTTAM (Koç University Research Center for Translational Medicine)
dc.contributor.departmentSchool of Medicine
dc.contributor.kuauthorEren, Candan Yasemin
dc.contributor.kuauthorEser, Hale Yapıcı
dc.contributor.kuauthorYigit, Arya
dc.contributor.schoolcollegeinstituteResearch Center
dc.contributor.schoolcollegeinstituteSCHOOL OF MEDICINE
dc.date.accessioned2024-11-09T12:31:46Z
dc.date.issued2021
dc.description.abstractThe role of glucagon-like peptide 1 (GLP-1) in insulin-dependent signaling is well-known; GLP-1 enhances glucose-dependent insulin secretion and lowers blood glucose in diabetes. GLP-1 receptors (GLP-1R) are also widely expressed in the brain, and in addition to its role in neuroprotection, it affects reward pathways. This systematic review aimed to analyze the studies on GLP-1 and reward pathways and its currently identified mechanisms. Methods: "Web of Science" and "Pubmed" were searched to identify relevant studies using GLP-1 as the keyword. Among the identified 26,539 studies, 30 clinical, and 71 preclinical studies were included. Data is presented by grouping rodent studies on palatable food intake, drugs of abuse, and studies on humans focusing on GLP-1 and reward systems. Results: GLP-1Rs are located in reward-related areas, and GLP-1, its agonists, and DPP-IV inhibitors are effective in decreasing palatable food intake, along with reducing cocaine, amphetamine, alcohol, and nicotine use in animals. GLP-1 modulates dopamine levels and glutamatergic neurotransmission, which results in observed behavioral changes. In humans, GLP-1 alters palatable food intake and improves activity deficits in the insula, hypothalamus, and orbitofrontal cortex (OFC). GLP-1 reduces food cravings partially by decreasing activity to the anticipation of food in the left insula of obese patients with diabetes and may inhibit overeating by increasing activity to the consumption of food in the right OFC of obese and left insula of obese with diabetes. Conclusion: current preclinical studies support the view that GLP-1 can be a target for reward system related disorders. More translational research is needed to evaluate its efficacy on human reward system related disorders.
dc.description.fulltextYES
dc.description.indexedbyWOS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.openaccessYES
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.sponsorshipN/A
dc.description.versionPublisher version
dc.description.volume14
dc.identifier.doi10.3389/fnbeh.2020.614884
dc.identifier.embargoNO
dc.identifier.filenameinventorynoIR02698
dc.identifier.issn1662-5153
dc.identifier.quartileN/A
dc.identifier.scopus2-s2.0-85100559120
dc.identifier.urihttps://hdl.handle.net/20.500.14288/1951
dc.identifier.wos613274200001
dc.keywordsGLP-1
dc.keywordsReward
dc.keywordsFood intake
dc.keywordsMood
dc.keywordsCocaine
dc.keywordsAmphetamine
dc.keywordsAlcohol
dc.keywordsNicotine
dc.language.isoeng
dc.publisherFrontiers
dc.relation.grantnoNA
dc.relation.ispartofFrontiers in Behavioral Neuroscience
dc.relation.urihttp://cdm21054.contentdm.oclc.org/cdm/ref/collection/IR/id/9344
dc.subjectMedicine
dc.subjectBehavioral sciences
dc.subjectNeurosciences and neurology
dc.titleCan GLP-1 be a target for reward system related disorders? a qualitative synthesis and systematic review analysis of studies on palatable food, drugs of abuse, and alcohol
dc.typeReview
dspace.entity.typePublication
local.contributor.kuauthorEser, Hale Yapıcı
local.contributor.kuauthorEren, Candan Yasemin
local.contributor.kuauthorYigit, Arya
local.publication.orgunit1SCHOOL OF MEDICINE
local.publication.orgunit1Research Center
local.publication.orgunit2KUTTAM (Koç University Research Center for Translational Medicine)
local.publication.orgunit2School of Medicine
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relation.isOrgUnitOfPublicationd02929e1-2a70-44f0-ae17-7819f587bedd
relation.isOrgUnitOfPublication.latestForDiscovery91bbe15d-017f-446b-b102-ce755523d939
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