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Article: High dosage of Exendin-4 increased early insulin secretion in differentiated beta cells from mouse embryonic stem cells

TitleHigh dosage of Exendin-4 increased early insulin secretion in differentiated beta cells from mouse embryonic stem cells
Authors
KeywordsBeta cells
Diabetes
Differentiation
Early insulin secretion
Embryonic stem cells
Exendin-4
Issue Date2010
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html
Citation
Acta Pharmacologica Sinica, 2010, v. 31 n. 5, p. 570-577 How to Cite?
AbstractAim: To investigate early insulin release (EIR) and late insulin release (LIR) upon glucose challenge as well as important insulin signaling factors in differentiated insulin-producing cells from embryonic stem cells(ESCs).Methods: A recently published protocol was modified by increasing the concentration of Exendin-4 (from 0.1 nmol/L to 10 nmol/L) together with an additional 5-day culture in low glucose (5.5 mmol/L) medium after differentiation. Gene expression profile, insulin content, C-peptide, EIR and LIR were determined. Results: Compared to a lower concentration of Exendin-4 (0.1 nmol/L), a higher concentration of Exendin-4 (10 nmol/L) increased glucose-responsive insulin secretion, especially EIR. Moreover, 10 nmol/L Exendin-4 increased the expression of the following genes: insulin 1, Pdx-1 (an important transcription factor, newly recognized insulin signaling factors), Epac1 and Epac2 (exchange proteins directly activated by cAMP 1 and 2), and sulfonylurea receptor 1 (SUR1, the subunit of the K ATP channel).Conclusion: According to current knowledge, our modified protocol with a higher concentration of Exendin-4 (10 nmol/L) together with an additional 5-day 5.5 mmol/L glucose culture after differentiation improved the efficiency of differentiation toward the beta cell phenotype, which was possibly the result of stimulated expression of Pdx-1, Epac 1, and Epac 2, which in turn inhibited the K(ATP) channel through combination with SUR1, leading to increased EIR upon glucose challenge. © 2010 CPS and SIMM All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/132180
ISSN
2015 Impact Factor: 3.166
2015 SCImago Journal Rankings: 1.161
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Hen_HK
dc.contributor.authorLam, Aen_HK
dc.contributor.authorXu, AMen_HK
dc.contributor.authorSl Lam, Ken_HK
dc.contributor.authorKim Chung, Sen_HK
dc.date.accessioned2011-03-21T08:59:25Z-
dc.date.available2011-03-21T08:59:25Z-
dc.date.issued2010en_HK
dc.identifier.citationActa Pharmacologica Sinica, 2010, v. 31 n. 5, p. 570-577en_HK
dc.identifier.issn1671-4083en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132180-
dc.description.abstractAim: To investigate early insulin release (EIR) and late insulin release (LIR) upon glucose challenge as well as important insulin signaling factors in differentiated insulin-producing cells from embryonic stem cells(ESCs).Methods: A recently published protocol was modified by increasing the concentration of Exendin-4 (from 0.1 nmol/L to 10 nmol/L) together with an additional 5-day culture in low glucose (5.5 mmol/L) medium after differentiation. Gene expression profile, insulin content, C-peptide, EIR and LIR were determined. Results: Compared to a lower concentration of Exendin-4 (0.1 nmol/L), a higher concentration of Exendin-4 (10 nmol/L) increased glucose-responsive insulin secretion, especially EIR. Moreover, 10 nmol/L Exendin-4 increased the expression of the following genes: insulin 1, Pdx-1 (an important transcription factor, newly recognized insulin signaling factors), Epac1 and Epac2 (exchange proteins directly activated by cAMP 1 and 2), and sulfonylurea receptor 1 (SUR1, the subunit of the K ATP channel).Conclusion: According to current knowledge, our modified protocol with a higher concentration of Exendin-4 (10 nmol/L) together with an additional 5-day 5.5 mmol/L glucose culture after differentiation improved the efficiency of differentiation toward the beta cell phenotype, which was possibly the result of stimulated expression of Pdx-1, Epac 1, and Epac 2, which in turn inhibited the K(ATP) channel through combination with SUR1, leading to increased EIR upon glucose challenge. © 2010 CPS and SIMM All rights reserved.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.htmlen_HK
dc.relation.ispartofActa Pharmacologica Sinicaen_HK
dc.subjectBeta cellsen_HK
dc.subjectDiabetesen_HK
dc.subjectDifferentiationen_HK
dc.subjectEarly insulin secretionen_HK
dc.subjectEmbryonic stem cellsen_HK
dc.subjectExendin-4en_HK
dc.subject.meshEmbryonic Stem Cells - cytology-
dc.subject.meshHypoglycemic Agents - pharmacology-
dc.subject.meshInsulin - metabolism-
dc.subject.meshPeptides - pharmacology-
dc.subject.meshVenoms - pharmacology-
dc.titleHigh dosage of Exendin-4 increased early insulin secretion in differentiated beta cells from mouse embryonic stem cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1671-4083&volume=31&issue=5&spage=570–577&epage=&date=2010&atitle=High+dosage+of+Exendin-4+increased+early+insulin+secretion+in+differentiated+beta+cells+from+mouse+embryonic+stem+cells-
dc.identifier.emailXu, AM:amxu@hkucc.hku.hken_HK
dc.identifier.emailKim Chung, S:skchung@hkucc.hku.hken_HK
dc.identifier.authorityXu, AM=rp00485en_HK
dc.identifier.authorityKim Chung, S=rp00381en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1038/aps.2010.38en_HK
dc.identifier.pmid20418895-
dc.identifier.scopuseid_2-s2.0-77952014233en_HK
dc.identifier.hkuros178229en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77952014233&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue5en_HK
dc.identifier.spage570en_HK
dc.identifier.epage577en_HK
dc.identifier.isiWOS:000277661600007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, H=36078286800en_HK
dc.identifier.scopusauthoridLam, A=7201848036en_HK
dc.identifier.scopusauthoridXu, AM=7202655409en_HK
dc.identifier.scopusauthoridSl Lam, K=36673897800en_HK
dc.identifier.scopusauthoridKim Chung, S=7404292976en_HK

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