Group space scan of flavor symmetries for nearly tribimaximal lepton mixing

We present a systematic group space scan of discrete Abelian flavor symmetries for lepton mass models that produce nearly tribimaximal lepton mixing. In our models, small neutrino masses are generated by the type-I seesaw mechanism. The lepton mass matrices emerge from higher-dimension operators via the Froggatt-Nielsen mechanism and are predicted as powers of a single expansion parameter \epsilon that is of the order of the Cabibbo angle \theta_C\simeq 0.2. We focus on solutions that can give close to tribimaximal lepton mixing with a very small reactor angle \theta_{13}\approx 0 and find several thousand explicit such models that provide an excellent fit to current neutrino data. The models are rather general in the sense that large leptonic mixings can come from the charged leptons and/or neutrinos. Moreover, in the neutrino sector, both left- and right-handed neutrinos can mix maximally. We also find a new relation \theta_{13}\lesssim\epsilon^3 for the reactor angle and a new sum rule \theta_{23}\approx\pi/4+\epsilon/\sqrt{2} for the atmospheric angle, allowing the models to be tested in future neutrino oscillation experiments.Comment: 18 pages, 2 tables, 2 figures, references added, final version to appear in JHE

Lipolysis drives expression of the constitutively active receptor GPR3 to induce adipose thermogenesis

Thermogenic adipocytes possess a therapeutically appealing, energy-expending capacity, which is canonically cold-induced by ligand-dependent activation of beta-adrenergic G protein-coupled receptors (GPCRs). Here, we uncover an alternate paradigm of GPCR-mediated adipose thermogenesis through the constitutively active receptor, GPR3. We show that the N terminus of GPR3 confers intrinsic signaling activity, resulting in continuous Gscoupling and cAMP production without an exogenous ligand. Thus, transcriptional induction of Gpr3 represents the regulatory parallel to ligand-binding of conventional GPCRs. Consequently, increasing Gpr3 expression in thermogenic adipocytes is alone sufficient to drive energy expenditure and counteract metabolic disease in mice. Gpr3 transcription is cold-stimulated by a lipolytic signal, and dietary fat potentiates GPR3-dependent thermogenesis to amplify the response to caloric excess. Moreover, we find GPR3 to be an essential, adrenergic-independent regulator of human brown adipocytes. Taken together, our findings reveal a noncanonical mechanism of GPCR control and thermogenic activation through the lipolysis-induced expression of constitutively active GPR3.Diabetes mellitus: pathophysiological changes and therap