{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen YC"],"funding":["Wellcome Trust"],"pagination":["102123"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12090325"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["96"],"pubmed_abstract":["<h4>Objectives</h4>Carriers of PAM (peptidylglycine alpha-amidating monooxygenase) coding variant alleles have reduced insulinogenic index, higher risk of developing type 2 diabetes (T2D), and islets from heterozygous carriers of the PAM p.Asp563Gly variant display reduced insulin secretion. Exactly how global PAM deficiency contributes to hyperglycemia remains unclear. PAM is the only enzyme capable of converting glycine-extended peptide hormones into amidated products. Like neuropeptide Y (NPY), α-melanocyte stimulating hormone (αMSH), and glucagon-like peptide 1 (GLP-1), islet amyloid polypeptide (IAPP), a beta cell peptide that forms islet amyloid in type 2 diabetes, is a PAM substrate. We hypothesized that Pam deficiency limited to beta cells would lead to reduced insulin secretion, p"],"journal":["Molecular metabolism"],"pubmed_title":["Peptidylglycine alpha-amidating monooxygenase is important in mice for beta-cell cilia formation and insulin secretion but promotes diabetes risk through beta-cell independent mechanisms."],"pmcid":["PMC12090325"],"funding_grant_id":["200837"],"pubmed_authors":["MacDonald PE","Xiong L","Back NE","Gloyn AL","Chen YC","Eipper BA","Zhen J","Komba M","Verchere CB","Mains RE"],"additional_accession":[]},"is_claimable":false,"name":"Peptidylglycine alpha-amidating monooxygenase is important in mice for beta-cell cilia formation and insulin secretion but promotes diabetes risk through beta-cell independent mechanisms.","description":"<h4>Objectives</h4>Carriers of PAM (peptidylglycine alpha-amidating monooxygenase) coding variant alleles have reduced insulinogenic index, higher risk of developing type 2 diabetes (T2D), and islets from heterozygous carriers of the PAM p.Asp563Gly variant display reduced insulin secretion. Exactly how global PAM deficiency contributes to hyperglycemia remains unclear. PAM is the only enzyme capable of converting glycine-extended peptide hormones into amidated products. Like neuropeptide Y (NPY), α-melanocyte stimulating hormone (αMSH), and glucagon-like peptide 1 (GLP-1), islet amyloid polypeptide (IAPP), a beta cell peptide that forms islet amyloid in type 2 diabetes, is a PAM substrate. We hypothesized that Pam deficiency limited to beta cells would lead to reduced insulin secretion, p","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jun","modification":"2026-06-01T06:18:37.841Z","creation":"2026-04-08T09:48:38.681Z"},"accession":"S-EPMC12090325","cross_references":{"pubmed":["40120979"],"doi":["10.1016/j.molmet.2025.102123"]}}