UCP2 mediates ghrelin's action on NPY/AgRP neurons by lowering free radicals

The gut-derived hormone ghrelin exerts its effect on the brain by regulating neuronal activity. Ghrelin-induced feeding behaviour is controlled by arcuate nucleus neurons that co-express neuropeptide Y and agouti-related protein (NPY/AgRP neurons). However, the intracellular mechanisms triggered by ghrelin to alter NPY/AgRP neuronal activity are poorly understood. Here we show that ghrelin initiates robust changes in hypothalamic mitochondrial respiration in mice that are dependent on uncoupling protein 2 (UCP2). Activation of this mitochondrial mechanism is critical for ghrelin-induced mitochondrial proliferation and electric activation of NPY/AgRP neurons, for ghrelin-triggered synaptic plasticity of pro-opiomelanocortin-expressing neurons, and for ghrelin-induced food intake. The UCP2-dependent action of ghrelin on NPY/AgRP neurons is driven by a hypothalamic fatty acid oxidation pathway involving AMPK, CPT1 and free radicals that are scavenged by UCP2. These results reveal a signalling modality connecting mitochondria-mediated effects of G-protein-coupled receptors on neuronal function and associated behaviour.     

Modified Dye for Water-Fast Ink-Jet Printing

A quaternary ammonium compound containing amino acid residue was synthesized by Converting 3-chloro-2-hydroxy-propyalkyldimethylammonium chlorides into its epoxide derivatives, then attaching an amino acid to the epoxide derivatives synthesized a quaternary ammonium compound containing amino acid residue. Modified dyes were prepared by the ionotropy of anionic dyes with the quaternary ammonium compound containing amino acid residue. It was discovered that the modified dyes exhibited an excellent pH controllable solubility. These modified dyes have good water solubility at pH> 8.0, but they were water insoluble at pH < 6.5. On the printing paper, modified dyes in water-based ink-jet print ink could convert to water insoluble form and give prints excellent water fastness.