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GIP_HUMAN [22–51] Peptide Encoded by the Glucose-Dependent Insulinotropic Polypeptide (GIP) Gene Suppresses Insulin Expression and Secretion in INS-1E Cells and Rat Pancreatic Islets

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cris.virtual.author-orcid0000-0002-3651-0972
cris.virtual.author-orcid0000-0001-9792-1145
cris.virtual.author-orcid0000-0003-0715-0223
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cris.virtual.author-orcid0000-0002-1948-6544
cris.virtual.author-orcid0000-0003-4059-1362
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cris.virtualsource.author-orcid652e209d-434a-47b3-b5fb-64c0aac5a84c
cris.virtualsource.author-orcid1815dbc7-82a3-4ce5-8dc9-bbe17826792b
cris.virtualsource.author-orcid0c22ceb5-e5c6-4f5d-a0fd-8ec91a16efa9
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cris.virtualsource.author-orcidb5ca3f7e-8c5b-47d7-b9c2-582f5ffa0e29
cris.virtualsource.author-orcid9118c61a-b066-4efc-a7af-486f9ebf9021
dc.abstract.enGIP_HUMAN [22–51] is a recently discovered peptide that shares the same precursor molecule with glucose-dependent insulinotropic polypeptide (GIP). In vivo, chronic infusion of GIP_HUMAN [22–51] in ApoE−/− mice enhanced the development of aortic atherosclerotic lesions and upregulated inflammatory and proatherogenic proteins. In the present study, we evaluate the effects of GIP_HUMAN [22–51] on insulin mRNA expression and secretion in insulin-producing INS-1E cells and isolated rat pancreatic islets. Furthermore, we characterize the influence of GIP_HUMAN [22–51] on cell proliferation and death and on Nf-kB nuclear translocation. Rat insulin-producing INS-1E cells and pancreatic islets, isolated from male Wistar rats, were used in this study. Gene expression was evaluated using real-time PCR. Cell proliferation was studied using a BrdU incorporation assay. Cell death was quantified by evaluating histone-complexed DNA fragments. Insulin secretion was determined using an ELISA test. Nf-kB nuclear translocation was detected using immunofluorescence. GIP_HUMAN [22–51] suppressed insulin (Ins1 and Ins2) in INS-1E cells and pancreatic islets. Moreover, GIP_HUMAN [22–51] promoted the translocation of NF-κB from cytoplasm to the nucleus. In the presence of a pharmacological inhibitor of NF-κB, GIP_HUMAN [22–51] was unable to suppress Ins2 mRNA expression. Moreover, GIP_HUMAN [22–51] downregulated insulin secretion at low (2.8 mmol/L) but not high (16.7 mmol/L) glucose concentration. By contrast, GIP_HUMAN [22–51] failed to affect cell proliferation and apoptosis. We conclude that GIP_HUMAN [22–51] suppresses insulin expression and secretion in pancreatic β cells without affecting β cell proliferation or apoptosis. Notably, the effects of GIP_HUMAN [22–51] on insulin secretion are glucose-dependent.
dc.affiliationWydział Medycyny Weterynaryjnej i Nauk o Zwierzętach
dc.affiliation.instituteKatedra Fizjologii, Biochemii i Biostruktury Zwierząt
dc.contributor.authorPusch, Emily
dc.contributor.authorKrążek, Małgorzata
dc.contributor.authorWojciechowicz, Tatiana
dc.contributor.authorSassek, Maciej
dc.contributor.authorKołodziejski, Paweł
dc.contributor.authorStrowski, Mathias
dc.contributor.authorNowak, Krzysztof W.
dc.contributor.authorSkrzypski, Marek
dc.date.access2025-06-24
dc.date.accessioned2025-10-08T06:22:43Z
dc.date.available2025-10-08T06:22:43Z
dc.date.copyright2023-10-05
dc.date.issued2023
dc.description.abstract<jats:p>GIP_HUMAN [22–51] is a recently discovered peptide that shares the same precursor molecule with glucose-dependent insulinotropic polypeptide (GIP). In vivo, chronic infusion of GIP_HUMAN [22–51] in ApoE−/− mice enhanced the development of aortic atherosclerotic lesions and upregulated inflammatory and proatherogenic proteins. In the present study, we evaluate the effects of GIP_HUMAN [22–51] on insulin mRNA expression and secretion in insulin-producing INS-1E cells and isolated rat pancreatic islets. Furthermore, we characterize the influence of GIP_HUMAN [22–51] on cell proliferation and death and on Nf-kB nuclear translocation. Rat insulin-producing INS-1E cells and pancreatic islets, isolated from male Wistar rats, were used in this study. Gene expression was evaluated using real-time PCR. Cell proliferation was studied using a BrdU incorporation assay. Cell death was quantified by evaluating histone-complexed DNA fragments. Insulin secretion was determined using an ELISA test. Nf-kB nuclear translocation was detected using immunofluorescence. GIP_HUMAN [22–51] suppressed insulin (Ins1 and Ins2) in INS-1E cells and pancreatic islets. Moreover, GIP_HUMAN [22–51] promoted the translocation of NF-κB from cytoplasm to the nucleus. In the presence of a pharmacological inhibitor of NF-κB, GIP_HUMAN [22–51] was unable to suppress Ins2 mRNA expression. Moreover, GIP_HUMAN [22–51] downregulated insulin secretion at low (2.8 mmol/L) but not high (16.7 mmol/L) glucose concentration. By contrast, GIP_HUMAN [22–51] failed to affect cell proliferation and apoptosis. We conclude that GIP_HUMAN [22–51] suppresses insulin expression and secretion in pancreatic β cells without affecting β cell proliferation or apoptosis. Notably, the effects of GIP_HUMAN [22–51] on insulin secretion are glucose-dependent.</jats:p>
dc.description.accesstimeat_publication
dc.description.bibliographyil., bibliogr.
dc.description.financepublication_nocost
dc.description.financecost0,00
dc.description.if2,8
dc.description.number10
dc.description.points100
dc.description.versionfinal_published
dc.description.volume14
dc.identifier.doi10.3390/genes14101910
dc.identifier.issn2073-4425
dc.identifier.urihttps://sciencerep.up.poznan.pl/handle/item/5272
dc.identifier.weblinkhttp://www.mdpi.com/2073-4425/14/10/1910
dc.languageen
dc.relation.ispartofGenes
dc.relation.pagesart. 1910
dc.rightsCC-BY
dc.sciencecloudnosend
dc.share.typeOPEN_JOURNAL
dc.subject.enbeta cell
dc.subject.enGIP
dc.subject.enGIP_HUMAN [22–51]
dc.subject.eninsulin
dc.subject.enINS-1E
dc.subject.enpancreatic islet
dc.subject.enexpression
dc.titleGIP_HUMAN [22–51] Peptide Encoded by the Glucose-Dependent Insulinotropic Polypeptide (GIP) Gene Suppresses Insulin Expression and Secretion in INS-1E Cells and Rat Pancreatic Islets
dc.typeJournalArticle
dspace.entity.typePublication
oaire.citation.issue10
oaire.citation.volume14