Four lipidomics datasets (mouse liver, mouse pancreatic islets, mouse soleus muscle and mouse visceral adipose tissue), generated for the publication Mehl et al., "A multiorgan map of metabolic, signalling, and inflammatory pathways that coordinately control fasting glycemia in mice"

Mehl, Thorens et al present a multiomics study aimiing to identify the pathways that are coordinately regulated in pancreatic b-cells, muscle, liver, and fat to control fasting glycemia we fed C57Bl/6, DBA/2 and Balb/c mice a regular chow or a high fat diet for 3, 10 and 30 days. We measured fasted glycemia, insulinemia and whole-body insulin resistance. Transcriptomic and lipidomic analysis were used in a data fusion approach to identify organ-specific pathways related to the glycemic levels across all conditions investigated. In pancreatic islets, constant insulinemia despite higher glycemic levels were associated with reduced expression of mRNAs encoding hormone and neurotransmitter receptors as well as OXPHOS, cadherins, integrins and gap junction proteins. Higher glycemia and whole-body insulin resistance were associated, in muscle, with reduced expression of mRNAs encoding insulin signaling proteins and enzymes of the glycolysis, Krebs’ cycle and OXPHOS pathways, as well as endocytosis and exocytosis proteins; in hepatocytes, with lower expression of mRNAs of the insulin signaling pathway, of branched chain amino acid catabolism and of OXPHOS; in adipose tissue, with increased expression of mRNAs of innate immunity and lipid catabolism. These data provide a map of the pathways that are coordinately recruited in the investigated tissues to control fasting glycemia and a resource for further studies of interorgan communication in glucose homeostasis.