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A genetically sensitized drug screen identifies a circadian diabetes target and establishes a novel discovery pathway to treat β-cell failure.

A mouse model of maturity-onset diabetes of the young illuminates that overactive TALK-1 channels limit β-cell calcium influx through membrane potential hyperpolarization, which blunts insulin secretion and causes glucose intolerance.

The structure provides key insights into hormone recognition and activation of the glucose-dependent insulinotropic polypeptide receptor.

Leptin acts cell autonomously on brainstem neurons that express GLP-1 to suppress development of excitatory viscerosensory inputs to the hypothalamus.

Pancreatic α and β cells have different cell autonomous signatures; this explains why α but not β cells can clear infections by potentially diabetogenic viruses.

Glucocorticoid receptor directly regulates the transcriptional activity of peroxisome proliferator-activated alpha (PPARα) before birth in anticipation of the sudden shifts in the postnatal nutrient source and metabolic demands.

Mutagenesis and activity assays in vitro and in vivo identify residues in the tethered agonist of GPR116, as well as those within the extracellular loops, that are critical for mediating the response to the tethered agonist.

Agonist and antagonist peptides of the corticotropin-releasing factor receptor type 1 adopt different folds and stabilize distinct conformations of the receptor transmembrane domain, which involves tilting of helices VI and VII around conserved glycine hinges.

The vasopressin type 2 receptor promotes dual Gα_s and Gα_q/11 signaling at early endosomes in β-arrestin-dependent and -independent manners.

The dodecahelical membrane anchors of mammalian adenylyl cyclase isoforms are receptors for unsaturated free fatty acids and, as a tonic signal, enhance or attenuate GPCR/Gsα-stimulated cyclic AMP formation.