Effect of Obesity-Induced Tumor Necrosis Factor Alpha on Adipocyte Function

Obesity-induced inflammation has been linked to the onset of insulin resistance (IR), which is a strong risk factor for the development of T2DM. Recent studies have indicated that tumor necrosis factor alpha (TNFα) plays a causative role in obesity-mediated IR via its overexpression in adipose tissue. Moreover, TNFα has been shown to induce the IR and the alteration of lipid and glucose metabolism in adipose tissue at various levels including normal adipocyte differentiation and mature adipocyte function. However, the mechanisms linking TNFα-induced adipocyte dysfunction in chronic obesity to the IR and T2DM are largely unknown. Herein we report that TNFα inhibited the mRNA expression of PPARγ, which is a key nuclear transcriptional factor for driving preadipocyte differentiation and maintaining normal function of mature adipocyte. TNFα treatment suppressed preadipocyte differentiation by downregulating mRNAs for FAS, perilipin, GLUT4, adiponectin, PGC-1α and C/EBPα and also altered adipocyte function by inhibiting mRNAs for perilipin, GLUT4, CPT-1 and PGC-1α, while increasing the expression of IL-6 and MCP1 mRNAs. In palmitic acid (PA)-induced in vitro hypertrophic adipocytes, we found that mRNA expression of inflammatory cytokines (TNFα and IL-6) was significantly elevated, while the expression of mRNAs for PPARγ, perilipin and adiponectin was markedly reduced, suggesting that TNFα may induce dysfunctional adipocyte phenotypes by targeting PPARγ and its target genes. In in vivo study, mice fed high fat diet (HFD) for 16 weeks had adipose tissue dysfunction as reflected by significant reduction of protein expression for PPARγ, perilipin, FAS and FABP4, consistent with the results observed in in vitro hypertrophic adipocytes. Interestingly, this was reversed by the loss of TNFα in TNFα knockout mice, indicating that TNFα may induce adipocyte dysfunction via the inhibition of PPARγ and its target genes. In the liver, HFD significantly increased hepatic triglyceride (TG) contents, while decreasing de novo lipogenesis (SCD1 and FAS), whereas TNFα deficiency decreased TG content and de novo lipogenesis compared to HFD-fed wild-type (WT) mice, suggesting that TNFα-induced adipocyte dysfunction is associated with hepatic lipid deposition in chronic obesity. Taken together, the current findings provide new insights into the role of TNFα in obesity-induced inflammation and also suggest the TNFα as a mediator for obesity-induced IR & T2D

Power dissipation analysis of PV module under partial shading

Photovoltaic (PV) generation has been growing dramatically over the last years and it ranges from small, rooftop-mounted or building integrated systems, to large utility scale power stations. Especially for rooftop-mounted PV system, PV modules are serially connected to match with PV inverter input voltage specification. For serially connected PV system, shading is a problem since the shaded PV module reduces the output whole string of PV modules. The excess power from the unshaded PV module is dissipated in the shaded PV module. In this paper, power dissipation of PV module under partial shading is analyzed with circuit analysis for series connected PV modules. The specific current and voltage operating point of the shaded PV module are analyzed under shading. PSIM simulation tool is used to verify the power dissipation analysis. When there is no bypass diode and three solar modules are connected in series, upto 39.1% of the total maximum PV power is dissipated in the shaded PV module. On the other hand, when the bypass is attached, 0.3% of the total maximum power is generated as a loss in the shaded PV module. The proposed analysis technique of shaded PV module could be used in PV system performance analysis, especially for maximum power point tracking (MPPT) performance

Origin of the increased velocities of domain wall motions in soft magnetic thin-film nanostripes beyond the velocity-breakdown regime

It is known that oscillatory domain-wall (DW) motions in soft magnetic thin-film nanostripes above the Walker critical field lead to a remarkable reduction in the average DW velocities. In a much-higher-field region beyond the velocity-breakdown regime, however, the DW velocities have been found to increase in response to a further increase of the applied field. We report on the physical origin and detailed mechanism of this unexpected behavior. We associate the mechanism with the serial dynamic processes of the nucleation of vortex-antivortex (V-AV) pairs inside the stripe or at its edges, the non-linear gyrotropic motions of Vs and AVs, and their annihilation process. The present results imply that a two-dimensional soliton model is required for adequate interpretation of DW motions in the linear- and oscillatory-DW-motion regimes as well as in the beyond-velocity-breakdown regime.Comment: 16 pages, 3 figure

Real-time observations of TRIP-induced ultrahigh strain hardening in a dual-phase CrMnFeCoNi high-entropy alloy.

Strategies involving metastable phases have been the basis of the design of numerous alloys, yet research on metastable high-entropy alloys is still in its infancy. In dual-phase high-entropy alloys, the combination of local chemical environments and loading-induced crystal structure changes suggests a relationship between deformation mechanisms and chemical atomic distribution, which we examine in here in a Cantor-like Cr20Mn6Fe34Co34Ni6 alloy, comprising both face-centered cubic (fcc) and hexagonal closed packed (hcp) phases. We observe that partial dislocation activities result in stable three-dimensional stacking-fault networks. Additionally, the fraction of the stronger hcp phase progressively increases during plastic deformation by forming at the stacking-fault network boundaries in the fcc phase, serving as the major source of strain hardening. In this context, variations in local chemical composition promote a high density of Lomer-Cottrell locks, which facilitate the construction of the stacking-fault networks to provide nucleation sites for the hcp phase transformation