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Search: WFRF:(Tuomi TiinaMaija) > (2020-2024) > An insulin hypersec...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003974naa a2200541 4500
001oai:lup.lub.lu.se:73cd2060-9df2-4d0f-b857-e02f245d3235
003SwePub
008230221s2023 | |||||||||||000 ||eng|
0247 a https://lup.lub.lu.se/record/73cd2060-9df2-4d0f-b857-e02f245d32352 URI
0247 a https://doi.org/10.1016/j.stem.2022.12.0012 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
1001 a Hermann, Florian M.u University of Copenhagen4 aut
2451 0a An insulin hypersecretion phenotype precedes pancreatic β cell failure in MODY3 patient-specific cells
264 1b Elsevier BV,c 2023
520 a MODY3 is a monogenic hereditary form of diabetes caused by mutations in the transcription factor HNF1A. The patients progressively develop hyperglycemia due to perturbed insulin secretion, but the pathogenesis is unknown. Using patient-specific hiPSCs, we recapitulate the insulin secretion sensitivity to the membrane depolarizing agent sulfonylurea commonly observed in MODY3 patients. Unexpectedly, MODY3 patient-specific HNF1A+/R272C β cells hypersecrete insulin both in vitro and in vivo after transplantation into mice. Consistently, we identified a trend of increased birth weight in human HNF1A mutation carriers compared with healthy siblings. Reduced expression of potassium channels, specifically the KATP channel, in MODY3 β cells, increased calcium signaling, and rescue of the insulin hypersecretion phenotype by pharmacological targeting ATP-sensitive potassium channels or low-voltage-activated calcium channels suggest that more efficient membrane depolarization underlies the hypersecretion of insulin in MODY3 β cells. Our findings identify a pathogenic mechanism leading to β cell failure in MODY3.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes0 (SwePub)302052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes0 (SwePub)302052 hsv//eng
653 a calcium signaling
653 a congenital hyperinsulinemia
653 a disease modeling
653 a HNF1A
653 a HNF4A
653 a K channel
653 a membrane potential
653 a MODY3
653 a pancreatic β cell
653 a patient-specific hiPSCs
7001 a Kjærgaard, Maya Friisu University of Copenhagen4 aut
7001 a Tian, Chengleiu University of Copenhagen,Helmholtz Zentrum München4 aut
7001 a Tiemann, Ulfu University of Copenhagen4 aut
7001 a Jackson, Abigailu University of Copenhagen4 aut
7001 a Olsen, Lars Rønnu Technical University of Denmark4 aut
7001 a Kraft, Mariau Lund University,Lunds universitet,Stamcellscentrum (SCC),Avdelningen för stamcellsforskning,Institutionen för laboratoriemedicin,Medicinska fakulteten,Stem Cell Center,Division of stem cell research,Department of Laboratory Medicine,Faculty of Medicine4 aut0 (Swepub:lu)molm-men
7001 a Carlsson, Per Olau Uppsala University4 aut
7001 a Elfving, Iina M.u Folkhälsan Research Center4 aut
7001 a Kettunen, Jarno L.T.u Helsinki University Central Hospital,Folkhälsan Research Center,University of Helsinki4 aut
7001 a Tuomi, Tiinamaijau Helsinki University Central Hospital,University of Helsinki,Folkhälsan Research Center4 aut
7001 a Novak, Ivanau University of Copenhagen4 aut
7001 a Semb, Henriku Helmholtz Zentrum München,University of Copenhagen4 aut0 (Swepub:lu)endo-hse
7102 a University of Copenhagenb Helmholtz Zentrum München4 org
7730 t Cell Stem Celld : Elsevier BVg 30:1, s. 8-51q 30:1<8-51x 1934-5909
8564 u http://dx.doi.org/10.1016/j.stem.2022.12.001x freey FULLTEXT
8564 8u https://lup.lub.lu.se/record/73cd2060-9df2-4d0f-b857-e02f245d3235
8564 8u https://doi.org/10.1016/j.stem.2022.12.001

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