<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lee KL</submitter><funding>Lottery Health New Zealand</funding><funding>Maurice Wilkins Centre for Molecular BioDiscovery</funding><funding>Ministry of Business, Innovation and Employment</funding><funding>Health Research Council of New Zealand</funding><pagination>14-22</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8632304</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><pubmed_abstract>Pancreatic islet-cell function and volume are both key determinants of the maintenance of metabolic health. Insulin resistance and islet-cell dysfunction often occur in the earlier stages of type 2 diabetes (T2D) progression. The ability of the islet cells to respond to insulin resistance by increasing hormone output accompanied by increased islet-cell volume is key to maintaining blood glucose control and preventing further disease progression. Eventual β-cell loss is the main driver of full-blown T2D and insulin-dependency. Researchers are targeting T2D with approaches that include those aimed at enhancing the function of the patient's existing β-cell population, or replacing islet β-cells. Another approach is to look for agents that enhance the natural capacity of the β-cell population </pubmed_abstract><journal>Islets</journal><pubmed_title>Vesiculin derived from IGF-II drives increased islet cell mass in a mouse model of pre-diabetes.</pubmed_title><pmcid>PMC8632304</pmcid><funding_grant_id>03/190</funding_grant_id><funding_grant_id>3626585</funding_grant_id><funding_grant_id>UOAX9902; PMIX0201; UOAX0815</funding_grant_id><funding_grant_id>3602434</funding_grant_id><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Montgomery K</pubmed_authors><pubmed_authors>Aitken JF</pubmed_authors><pubmed_authors>Williams GM</pubmed_authors><pubmed_authors>Cooper GJS</pubmed_authors><pubmed_authors>Lee KL</pubmed_authors><pubmed_authors>Brimble MA</pubmed_authors><pubmed_authors>Hsu HL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Vesiculin derived from IGF-II drives increased islet cell mass in a mouse model of pre-diabetes.</name><description>Pancreatic islet-cell function and volume are both key determinants of the maintenance of metabolic health. Insulin resistance and islet-cell dysfunction often occur in the earlier stages of type 2 diabetes (T2D) progression. The ability of the islet cells to respond to insulin resistance by increasing hormone output accompanied by increased islet-cell volume is key to maintaining blood glucose control and preventing further disease progression. Eventual β-cell loss is the main driver of full-blown T2D and insulin-dependency. Researchers are targeting T2D with approaches that include those aimed at enhancing the function of the patient's existing β-cell population, or replacing islet β-cells. Another approach is to look for agents that enhance the natural capacity of the β-cell population </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jan</publication><modification>2025-04-26T16:04:43.623Z</modification><creation>2022-02-11T13:59:51.326Z</creation></dates><accession>S-EPMC8632304</accession><cross_references><pubmed>34632959</pubmed><doi>10.1080/19382014.2021.1982326</doi></cross_references></HashMap>