Effect of FeSO4 treatment on glucose metabolism in diabetic rats

Iron, the prosthetic group of haemoglobin, was found to lower serum glucose levels of diabetic rats. Its regulative mechanism and effects on enzymatic activities of glucose metabolism are still unknown. In this study, the correlation between iron supply and enzymatic activities of glucose metabolism and respiratory chain were evaluated in liver and kidney tissues of alloxan induced-diabetic rats. After FeSO₄ and metformin administration, serum samples were collected for serum glucose and fructosamine level measurements. Kidney and liver tissues were excised at the end of the study for assaying enzymatic activities of isocitrate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADH-dehydrogenase and cytochrome-c-oxidase. Results showed significantly decreased serum glucose and fructosamine levels in treatment groups and enhanced enzymatic activities of several proteins as compared with the diabetic control group. Therefore, these data suggested that FeSO₄ administration could increase the supply of oxygen, enhance enzymatic activities of glucose metabolism and the respiratory chain, accelerate glucose metabolism and consequently decrease serum glucose levels.     

What confines an annual plant to two separate zones along coastal topographic gradients?

We investigated the roles of flooding, salinity, and plant competition in creating a bimodal zonation pattern of the marsh dominant annual plant, Suaeda salsa, along coastal topographic gradients on the Pacific coast of northern China. In two consecutive years, we manipulated salinity and flooding, salinity, and competition for S. salsa seedlings that had been transplanted into the mudflat, the high marsh, and the upland, respectively. S. salsa plants that had been transplanted into the mudflat were completely eliminated in the non-elevated treatments whereas they performed much better in the 10 cm elevated treatments, regardless of salinity treatments. Although the performance of S. salsa transplanted into the high marsh did not differ between the fresh (watered) and the salt (control) treatments, S. salsa seedling emergence in the high marsh was nearly completely inhibited in the salt treatments. In contrast, a large number of S. salsa seedlings did emerge in the fresh treatments. S. salsa transplanted into the upland performed well when neighbors were removed, whereas it appeared to be strongly suppressed when neighbors were present. These data indicated that flooding, salinity, and competition all played a role in determining the zonation pattern of S. salsa. Furthermore, the importance of salinity was found to vary with life-history stage. Based on the results from these field manipulative experiments, we suggest that the marsh plant zonation paradigm may hold true for plant distributions along landscape-scale topographic gradients from mudflats to uplands in general. The relative importance of flooding, salinity, and competition, however, may vary at different elevations within a site and between sites. Handling editor: Pierluigi Viaroli     

Acylation-stimulating protein/C5L2-neutralizing antibodies alter triglyceride metabolism in vitro and in vivo

Acylation-stimulating protein (ASP), a lipogenic hormone, stimulates triglyceride (TG) synthesis and glucose transport upon activation of C5L2, a G protein-coupled receptor. ASP-deficient mice have reduced adipose tissue mass due to increased energy expenditure despite increased food intake. The objective of this study was to evaluate the blocking of ASP-C5L2 interaction via neutralizing antibodies (anti-ASP and anti-C5L2-L1 against C5L2 extracellular loop 1). In vitro, anti-ASP and anti-C5L2-L1 blocked ASP binding to C5L2 and efficiently inhibited ASP stimulation of TG synthesis and glucose transport. In vivo, neither anti-ASP nor anti-C5L2-L1 altered body weight, adipose tissue mass, food intake, or hormone levels (insulin, leptin, and adiponectin), but they did induce a significant delay in TG clearance [P < 0.0001, 2-way repeated-measures (RM) ANOVA] and NEFA clearance (P < 0.0001, 2-way RM ANOVA) after a fat load. After treatment with either anti-ASP or anti-C5L2-L1 antibody there was no change in adipose tissue AMPK activity, but neutralizing antibodies decreased perirenal TG mass (-38.4% anti-ASP, -18.8% anti-C5L2, P < 0.01-0.001) and perirenal LPL activity (-75.6% anti-ASP, -72.5% anti-C5L2, P < 0.05). In liver, anti-C5L2-L1 decreased TG mass (-42.8%, P < 0.05), whereas anti-ASP increased AMPK activity (+34.6%, P < 0.001). In the muscle, anti-C5L2-L1 significantly increased TG mass (+128.0%, P < 0.05), LPL activity (+226.1%, P < 0.001), and AMPK activity (+71.1%, P < 0.01). In addition, anti-ASP increased LPL activity (+164.4, P < 0.05) and AMPK activity (+53.9%, P < 0.05) in muscle. ASP/C5L2-neutralizing antibodies effectively block ASP-C5L2 interaction, altering lipid distribution and energy utilization.     

Probing the structural basis for differential KCNQ1 modulation by KCNE1 and KCNE2

KCNE1 associates with KCNQ1 to increase its current amplitude and slow the activation gating process, creating the slow delayed rectifier channel that functions as a “repolarization reserve” in human heart. The transmembrane domain (TMD) of KCNE1 plays a key role in modulating KCNQ1 pore conductance and gating kinetics, and the extracellular juxtamembrane (EJM) region plays a modulatory role by interacting with the extracellular surface of KCNQ1. KCNE2 is also expressed in human heart and can associate with KCNQ1 to suppress its current amplitude and slow the deactivation gating process. KCNE1 and KCNE2 share the transmembrane topology and a high degree of sequence homology in TMD and surrounding regions. The structural basis for their distinctly different effects on KCNQ1 is not clear. To address this question, we apply cysteine (Cys) scanning mutagenesis to TMDs and EJMs of KCNE1 and KCNE2. We analyze the patterns of functional perturbation to identify high impact positions, and probe disulfide formation between engineered Cys side chains on KCNE subunits and native Cys on KCNQ1. We also use methanethiosulfonate reagents to probe the relationship between EJMs of KCNE subunits and KCNQ1. Our data suggest that the TMDs of both KCNE subunits are at about the same location but interact differently with KCNQ1. In particular, the much closer contact of KCNE2 TMD with KCNQ1, relative to that of KCNE1, is expected to impact the allosteric modulation of KCNQ1 pore conductance and may explain their differential effects on the KCNQ1 current amplitude. KCNE1 and KCNE2 also differ in the relationship between their EJMs and KCNQ1. Although the EJM of KCNE1 makes intimate contacts with KCNQ1, there appears to be a crevice between KCNQ1 and KCNE2. This putative crevice may perturb the electrical field around the voltage-sensing domain of KCNQ1, contributing to the differential effects of KCNE2 versus KCNE1 on KCNQ1 gating kinetics.     

Proteomic analysis of effect of hyperthermia on spermatogenesis in adult male mice

We characterized cellular and molecular mechanisms involved in spermatogenesis following short-term heat exposure of murine testis. For these studies, we utilized a proteomic approach with two-dimensional gel electrophoresis (2DE) analyses and mass spectroscopic identification of proteins with altered expression in mouse testes at different times after heat shock. We established a proteome reference map from 7-wk-old mouse testis linked to a federated proteome database. We used these tools to analyze quantitative variations in the tissue over a time course of 0.5, 2, 6, and 12 h following heat exposure. We separated 108 protein spots expressed differentially between the heat shock tissues and the control mouse testes. Of these spots, we identified 36 by comparing with the control reference map. We then focused on the heterogeneous nuclear ribonucleoproteins (hnRNPs) and the chaperonins containing t-complex polypeptide-1 (CCT). Further analysis in this heat-shocked model suggests numerous potential mechanisms for heat shock-induced spermatogenic disorder.     

Solving the aerodynamics of fungal flight: how air viscosity slows spore motion

Viscous drag causes the rapid deceleration of fungal spores after high-speed launches and limits discharge distance. Stokes' law posits a linear relationship between drag force and velocity. It provides an excellent fit to experimental measurements of the terminal velocity of free-falling spores and other instances of low Reynolds number motion (Re<1). More complex, non-linear drag models have been devised for movements characterized by higher Re, but their effectiveness for modeling the launch of fast-moving fungal spores has not been tested. In this paper, we use data on spore discharge processes obtained from ultra-high-speed video recordings to evaluate the effects of air viscosity predicted by Stokes' law and a commonly used non-linear drag model. We find that discharge distances predicted from launch speeds by Stokes' model provide a much better match to measured distances than estimates from the more complex drag model. Stokes' model works better over a wide range projectile sizes, launch speeds, and discharge distances, from microscopic mushroom ballistospores discharged at <1 m s(-1) over a distance of <0.1mm (Re<1.0), to macroscopic sporangia of Pilobolus that are launched at >10 m s(-1) and travel as far as 2.5m (Re>100).