{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tornovsky-Babeay S"],"funding":["Robert M. and Marilyn Sternberg Family Charitable Foundation","NIDDK NIH HHS","National Institute of Diabetes and Digestive and Kidney Diseases","European Foundation for the Study of Diabetes","Ernest and Bonnie Beutler Research Program of Excellence in Genomic Medicine","British Israel Research Exchange","Israel Science Foundation","The Alex U Soyka pancreatic cancer fund","Waldholtz / Pakula family"],"pagination":["1133-1143"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8117185"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["64(5)"],"pubmed_abstract":["<h4>Aims/hypothesis</h4>Acute hyperglycaemia stimulates pancreatic beta cell proliferation in the mouse whereas chronic hyperglycaemia appears to be toxic. We hypothesise that this toxic effect is mediated by increased beta cell workload, unrelated to hyperglycaemia per se.<h4>Methods</h4>To test this hypothesis, we developed a novel mouse model of cell-autonomous increased beta cell glycolytic flux caused by a conditional heterozygous beta cell-specific mutation that activates glucokinase (GCK), mimicking key aspects of the rare human genetic disease GCK-congenital hyperinsulinism.<h4>Results</h4>In the mutant mice, we observed random and fasting hypoglycaemia (random 4.5-5.4 mmol/l and fasting 3.6 mmol/l) that persisted for 15 months. GCK activation led to increased beta cell proliferati"],"journal":["Diabetologia"],"pubmed_title":["Biphasic dynamics of beta cell mass in a mouse model of congenital hyperinsulinism: implications for type 2 diabetes."],"pmcid":["PMC8117185"],"funding_grant_id":["UC4 DK104119","T32 DK007314","UC4DK104119","14BX14NHBG","1782/18"],"pubmed_authors":["Tornovsky-Babeay S","Dor Y","Feleke E","Kaestner KH","Avrahami D","Glaser B","Weinberg-Corem N","Ben-Haroush Schyr R","Lavi J"],"additional_accession":[]},"is_claimable":false,"name":"Biphasic dynamics of beta cell mass in a mouse model of congenital hyperinsulinism: implications for type 2 diabetes.","description":"<h4>Aims/hypothesis</h4>Acute hyperglycaemia stimulates pancreatic beta cell proliferation in the mouse whereas chronic hyperglycaemia appears to be toxic. We hypothesise that this toxic effect is mediated by increased beta cell workload, unrelated to hyperglycaemia per se.<h4>Methods</h4>To test this hypothesis, we developed a novel mouse model of cell-autonomous increased beta cell glycolytic flux caused by a conditional heterozygous beta cell-specific mutation that activates glucokinase (GCK), mimicking key aspects of the rare human genetic disease GCK-congenital hyperinsulinism.<h4>Results</h4>In the mutant mice, we observed random and fasting hypoglycaemia (random 4.5-5.4 mmol/l and fasting 3.6 mmol/l) that persisted for 15 months. GCK activation led to increased beta cell proliferati","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 May","modification":"2025-04-04T10:16:51.347Z","creation":"2025-04-04T10:16:51.347Z"},"accession":"S-EPMC8117185","cross_references":{"pubmed":["33558985"],"doi":["10.1007/s00125-021-05390-x"]}}