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Conclusions/interpretation The association of several targeted proteins with fasting C-peptide/glucose levels in the first year after diagnosis suggests their connection with the underlying changes accompanying alterations in beta cell function in type 1 diabetes

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This study aimed to investigate the molecular mechanism by which the transcription factor CCAAT/enhancer-binding protein (C/EBP) regulates hepatic lipid accumulation through the miR-335-5pmediated PRKAA2/AMPK signaling pathway

Finally, our structures reveal mechanistic details of MC4R activation/inhibition, and provide important insights into the regulation of the receptor signaling profile which will facilitate the development of tailored anti-obesity drugs.