{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hedaya L"],"funding":["Qatar National Research Fund"],"pagination":["1296"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12384308"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(16)"],"pubmed_abstract":["N-lactoyl amino acids (Lac-AAs) are key players that regulate appetite and body weight. The most prominent and well-studied member is N-lactoyl phenylalanine (Lac-Phe), which can be induced by food intake, exercise and metformin treatment. However, its broader metabolic impact remains insufficiently characterized. This study investigates the effects of Lac-Phe on insulin signaling, inflammation, and mitochondrial respiration using HepG2 and differentiated C2C12 cell models, as well as isolated rat brain mitochondria and synaptosomes. Our results demonstrate that Lac-Phe significantly impairs insulin-stimulated phosphorylation of key proteins in the insulin signaling pathway, particularly in skeletal muscle cells, indicating disrupted insulin signaling. Additionally, Lac-Phe exposure increa"],"journal":["Cells"],"pubmed_title":["N-Lactoyl Phenylalanine Disrupts Insulin Signaling, Induces Inflammation, and Impairs Mitochondrial Respiration in Cell Models."],"pmcid":["PMC12384308"],"funding_grant_id":["ARG01-0420-230007"],"pubmed_authors":["Elashi AA","Davey GP","Elrayess MA","Hedaya L","Al-Asmakh M","Espino-Guarch M","Naja K","Anwardeen N","Aldirbashi OY","Almuraikhy S","Zughaier SM"],"additional_accession":[]},"is_claimable":false,"name":"N-Lactoyl Phenylalanine Disrupts Insulin Signaling, Induces Inflammation, and Impairs Mitochondrial Respiration in Cell Models.","description":"N-lactoyl amino acids (Lac-AAs) are key players that regulate appetite and body weight. The most prominent and well-studied member is N-lactoyl phenylalanine (Lac-Phe), which can be induced by food intake, exercise and metformin treatment. However, its broader metabolic impact remains insufficiently characterized. This study investigates the effects of Lac-Phe on insulin signaling, inflammation, and mitochondrial respiration using HepG2 and differentiated C2C12 cell models, as well as isolated rat brain mitochondria and synaptosomes. Our results demonstrate that Lac-Phe significantly impairs insulin-stimulated phosphorylation of key proteins in the insulin signaling pathway, particularly in skeletal muscle cells, indicating disrupted insulin signaling. Additionally, Lac-Phe exposure increa","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-04-08T10:37:18.682Z","creation":"2026-04-08T01:29:47.474Z"},"accession":"S-EPMC12384308","cross_references":{"pubmed":["40862774"],"doi":["10.3390/cells14161296"]}}