IL-33 promotes pancreatic ß-cell survival and insulin secretion under diabetogenic conditions through PPARγ.

Pancreatic ß-cell dysfunction plays a vital role in the development of diabetes. IL-33 exerts anti-diabetic effects via its anti-inflammatory properties and has been demonstrated to increase insulin secretion in animal models. However, IL-33, as a pleiotropic cytokine, may also exert a deleterious effect on ß-cells, which has not been rigorously studied. In the present study, we found that IL-33 promoted cell survival and insulin secretion in MIN6 (a mouse pancreatic ß-cell line) cells under diabetogenic conditions. IL-33 increased the expression of its receptor ST2 and the transcription factor PPARγ, whereas PPARγ inhibition impaired IL-33-mediated ß-cell survival and insulin release. IL-33 did not repress the expression of pro-inflammatory mediators, including Tf, Icam1, Cxcl10, and Il1b, whereas it significantly reduced the expression of Ccl2. IL-33 decreased TNF-α secretion and increased IL-10 secretion; these effects were completely reversed by PPARγ inhibition. IL-33 increased glucose uptake and expression of Glut2. It upregulated the expression of glycolytic enzyme genes, namely, Pkm2, Hk2, Gpi1, and Tpi, and downregulated the expression of Gck, Ldha, and Mct4. However, it did not alter hexokinase activity. Moreover, IL-33 increased the number and activity of mitochondria, accompanied by increased ATP production and reduced accumulation of ROS. IL-33 upregulated the expression of PGC-1α and cytochrome c, and mitochondrial fission- and fusion-associated genes, including Mfn1, Mfn2, and Dnm1l. IL-33-mediated mitochondrial homeostasis was partially reversed by PPARγ inhibition. Altogether, IL-33 protects ß-cell survival and insulin secretion that could be partially driven via PPARγ, which regulates glucose uptake and promotes mitochondrial function and anti-inflammatory responses.

Improved power generation using nitrogen-doped 3D graphite foam anodes in microbial fuel cells.

The properties of the anode material and structure are critical to the microbial growth and interfacial electron transfer between the biofilm and the anode. In this paper, we prepared the nitrogen-doped 3D expanded graphite foam (NEGF) by simple, rapid and inexpensive methods of liquid nitrogen expansion and hydrothermal treatment from commercial graphite foil (GF). X-ray photoelectron spectroscopy confirmed the success of nitrogen doping on expanded graphite foam (EGF). Using cyclic voltammetry and electrochemical impedance spectroscopy, the NEGF and EGF electrode exhibited increased electrochemical active surface area and fast interfacial electron transfer ability than that of pristine GF, and NEGF electrode performed even better. Scanning electron microscopy revealed that NEGF and EGF possessed graphene-like structure and large surface area. MFCs equipped with NEGF or EGF anodes, respectively, achieved maximum power density of 0.739 and 0.536 W m-2, which was about 17.4 and 12.6 times larger than that of MFCs with GF anodes (0.0451 W m-2). The anode and cathode polarization curves further confirmed that the different anode other than the cathode was responsible for the advanced performance of MFCs. The morphology of the biofilm on three kinds of anodes proved the densest biofilm formed on NEGF anode. All the results indicated the synergistic effect of 3D graphene-like structure and N-doped surface on the performance of MFCs, which might provide special insights into designing simple and efficient route for anode construction to achieve promising electricity generation.