Eugenol has the ability to improve the type 1 diabetes mellitus through NRF2-mediated oxidative stress pathway.

Metabolic abnormalities in hepatocytes cause the alteration of transcriptional profile and function of immune cells in the tissue microenvironment.

Mir802 serves as a pivotal mediator facilitating communication between adipose tissue and macrophages through the activation of NF-KB signaling pathways.

Loss of the Zinc transporter SLC39A5 protects from obesity-driven hyperglycemia and liver pathology.

Modelling O-GlcNAc transferase intellectual disability reveals the roles of this post-translational modification in regulating normal axonal terminal morphology and maintaining appropriate sleep homeostasis, pharmacological and genetic rescues of O-GlcNAcylation highlight the complexities of addressing this disorder.