Sn4 P3 is introduced for the first time as an anode material for Na-ion batteries. Sn4 P3 delivers a high reversible capacity of 718 mA h g(-1), and shows very stable cycle performance with negligible capa-city fading over 100 cycles, which is attributed to the confinement effect of Sn nanocrystallites in the amorphous phosphorus matrix during cycling.

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The controllable assembly behavior of diphenylalanine molecules to form nanowires (NWs) and nanotubes (NTs) and their structural details are presented (see figure). The nanoscale morphologies are closely related to molecular arrangements of diphenylalanine as revealed by Rietveld refinement of powder X‐ray diffraction patterns and electron‐density distributions in NTs and NWs via the maximum entropy method analysis.

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Peroxisome proliferator-activated receptor-α (PPARα) is a dietary lipid sensor, whose activation results in hypolipidemic effects. In this study, we investigated whether PPARα activation affects energy metabolism in white adipose tissue (WAT). Activation of PPARα by its agonist (bezafibrate) markedly reduced adiposity in KK mice fed a high-fat diet. In 3T3-L1 adipocytes, addition of GW7647, a highly specific PPARα agonist, during adipocyte differentiation enhanced glycerol-3-phosphate dehydrogenase activity, insulin-stimulated glucose uptake, and adipogenic gene expression. However, triglyceride accumulation was not increased by PPARα activation. PPARα activation induced expression of target genes involved in FA oxidation and stimulated FA oxidation. In WAT of KK mice treated with bezafibrate, both adipogenic and FA oxidation-related genes were significantly upregulated. These changes in mRNA expression were not observed in PPARα-deficient mice. Bezafibrate treatment enhanced FA oxidation in isolated adipocytes, suppressing adipocyte hypertrophy. Chromatin immunoprecipitation (ChIP) assay revealed that PPARα was recruited to promoter regions of both adipogenic and FA oxidation-related genes in the presence of GW7647 in 3T3-L1 adipocytes. These findings indicate that the activation of PPARα affects energy metabolism in adipocytes, and PPARα activation in WAT may contribute to the clinical effects of fibrate drugs.