{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Merz KE"],"funding":["NIDDK NIH HHS","U.S. Department of Health & Human Services | NIH | National Cancer Institute","Larry L. Hillblom Foundation","NCI NIH HHS","U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases"],"pagination":["424"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8776765"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Mitochondrial dysfunction is implicated in skeletal muscle insulin resistance. Syntaxin 4 (STX4) levels are reduced in human diabetic skeletal muscle, and global transgenic enrichment of STX4 expression improves insulin sensitivity in mice. Here, we show that transgenic skeletal muscle-specific STX4 enrichment (skmSTX4tg) in mice reverses established insulin resistance and improves mitochondrial function in the context of diabetogenic stress. Specifically, skmSTX4tg reversed insulin resistance caused by high-fat diet (HFD) without altering body weight or food consumption. Electron microscopy of wild-type mouse muscle revealed STX4 localisation at or proximal to the mitochondrial membrane. STX4 enrichment prevented HFD-induced mitochondrial fragmentation and dysfunction through a mechanism "],"journal":["Nature communications"],"pubmed_title":["Enrichment of the exocytosis protein STX4 in skeletal muscle remediates peripheral insulin resistance and alters mitochondrial dynamics via Drp1."],"pmcid":["PMC8776765"],"funding_grant_id":["R01 DK102233","#2020-D-018-FEL","P30CA33572","DK1129712","P30 CA033572","DK102233","R01 DK067912","DK067912"],"pubmed_authors":["Veluthakal R","Jiang L","Zhou C","Huss JM","Dai W","McCown EM","Hamilton A","Oh E","Thurmond DC","Merz KE","Fueger PT","Hwang J"],"additional_accession":[]},"is_claimable":false,"name":"Enrichment of the exocytosis protein STX4 in skeletal muscle remediates peripheral insulin resistance and alters mitochondrial dynamics via Drp1.","description":"Mitochondrial dysfunction is implicated in skeletal muscle insulin resistance. Syntaxin 4 (STX4) levels are reduced in human diabetic skeletal muscle, and global transgenic enrichment of STX4 expression improves insulin sensitivity in mice. Here, we show that transgenic skeletal muscle-specific STX4 enrichment (skmSTX4tg) in mice reverses established insulin resistance and improves mitochondrial function in the context of diabetogenic stress. Specifically, skmSTX4tg reversed insulin resistance caused by high-fat diet (HFD) without altering body weight or food consumption. Electron microscopy of wild-type mouse muscle revealed STX4 localisation at or proximal to the mitochondrial membrane. STX4 enrichment prevented HFD-induced mitochondrial fragmentation and dysfunction through a mechanism ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2025-05-29T21:30:16.51Z","creation":"2025-05-29T21:30:16.51Z"},"accession":"S-EPMC8776765","cross_references":{"pubmed":["35058456"],"doi":["10.1038/s41467-022-28061-w"]}}