{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Clark AL"],"funding":["BLRD VA","NIDDK NIH HHS","NHLBI NIH HHS","Korea National Institute of Health","NINDS NIH HHS","U.S. Department of Veterans Affairs"],"pagination":["2455-2465"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8490276"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(11)"],"pubmed_abstract":["Aims
Type 1 diabetes (T1D) has a strong genetic predisposition and requires an environmental trigger to initiate the beta-cell autoimmune destruction. The rate of childhood obesity has risen in parallel to the proportion of T1D, suggesting high-fat diet (HFD)/obesity as potential environmental triggers for autoimmune diabetes. To explore this, non-obese diabetic (NOD) mice were subjected to HFD and monitored for the development of diabetes, insulitis and beta-cell stress.Materials and methods
Four-week-old female NOD mice were placed on HFD (HFD-NOD) or standard chow-diet. Blood glucose was monitored weekly up to 40 weeks of age, and glucose- and insulin-tolerance tests performed at 4, 10 and 15 weeks. Pancreata and islets were analysed for insulin secretion, beta-cell mass"],"journal":["Diabetes, obesity & metabolism"],"pubmed_title":["High-fat diet prevents the development of autoimmune diabetes in NOD mice."],"pmcid":["PMC8490276"],"funding_grant_id":["R56 DK098584","T32 DK007120","R01 HL107594","P30 DK020579","I01BX004235","NS094692","HL 143431","R01 DK123163","R01DK123163","HL 107594","P30 DK056341","I01 BX004235","R56DK098584","R01 HL143431","R01 NS094692"],"pubmed_authors":["Remedi MS","Yan Z","Clark AL","Shi V","Chen SX","Kulkarni DH","Diwan A"],"additional_accession":[]},"is_claimable":false,"name":"High-fat diet prevents the development of autoimmune diabetes in NOD mice.","description":"Aims
Type 1 diabetes (T1D) has a strong genetic predisposition and requires an environmental trigger to initiate the beta-cell autoimmune destruction. The rate of childhood obesity has risen in parallel to the proportion of T1D, suggesting high-fat diet (HFD)/obesity as potential environmental triggers for autoimmune diabetes. To explore this, non-obese diabetic (NOD) mice were subjected to HFD and monitored for the development of diabetes, insulitis and beta-cell stress.Materials and methods
Four-week-old female NOD mice were placed on HFD (HFD-NOD) or standard chow-diet. Blood glucose was monitored weekly up to 40 weeks of age, and glucose- and insulin-tolerance tests performed at 4, 10 and 15 weeks. Pancreata and islets were analysed for insulin secretion, beta-cell mass","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Nov","modification":"2026-04-08T17:44:43.266Z","creation":"2025-02-18T23:36:37.338Z"},"accession":"S-EPMC8490276","cross_references":{"pubmed":["34212475"],"doi":["10.1111/dom.14486"]}}