{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kubrak O"],"funding":["Natur og Univers, Det Frie Forskningsråd (Natural Sciences, Danish Council for Independent Research)","Novo Nordisk Fonden (Novo Nordisk Foundation)","Natur og Univers, Det Frie Forskningsråd","Novo Nordisk Fonden"],"pagination":["6126"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11271308"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["Obesity impairs tissue insulin sensitivity and signaling, promoting type-2 diabetes. Although improving insulin signaling is key to reversing diabetes, the multi-organ mechanisms regulating this process are poorly defined. Here, we screen the secretome and receptome in Drosophila to identify the hormonal crosstalk affecting diet-induced insulin resistance and obesity. We discover a complex interplay between muscle, neuronal, and adipose tissues, mediated by Bone Morphogenetic Protein (BMP) signaling and the hormone Bursicon, that enhances insulin signaling and sugar tolerance. Muscle-derived BMP signaling, induced by sugar, governs neuronal Bursicon signaling. Bursicon, through its receptor Rickets, a Leucine-rich-repeat-containing G-protein coupled receptor (LGR), improves insulin secreti"],"journal":["Nature communications"],"pubmed_title":["LGR signaling mediates muscle-adipose tissue crosstalk and protects against diet-induced insulin resistance."],"pmcid":["PMC11271308"],"funding_grant_id":["8021-00055B","NNF21OC0070402","NNF22OC0078344"],"pubmed_authors":["Mazzoni G","Koyama T","Hansen JL","Halberg KV","Hansen JB","Texada MJ","Larsen MR","Jorgensen AF","Madsen D","Rewitz K","Kubrak O","Nagy S","Lassen M","Hald J"],"additional_accession":[]},"is_claimable":false,"name":"LGR signaling mediates muscle-adipose tissue crosstalk and protects against diet-induced insulin resistance.","description":"Obesity impairs tissue insulin sensitivity and signaling, promoting type-2 diabetes. Although improving insulin signaling is key to reversing diabetes, the multi-organ mechanisms regulating this process are poorly defined. Here, we screen the secretome and receptome in Drosophila to identify the hormonal crosstalk affecting diet-induced insulin resistance and obesity. We discover a complex interplay between muscle, neuronal, and adipose tissues, mediated by Bone Morphogenetic Protein (BMP) signaling and the hormone Bursicon, that enhances insulin signaling and sugar tolerance. Muscle-derived BMP signaling, induced by sugar, governs neuronal Bursicon signaling. Bursicon, through its receptor Rickets, a Leucine-rich-repeat-containing G-protein coupled receptor (LGR), improves insulin secreti","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-07-15T04:18:06.17Z","creation":"2025-04-19T13:12:27.39Z"},"accession":"S-EPMC11271308","cross_references":{"pubmed":["39033139"],"doi":["10.1038/s41467-024-50468-w"]}}