Metabolic profiles in the response to supplementation with composite antimicrobial peptides in piglets challenged with deoxynivalenol.

Deoxynivalenol (DON) causes various toxic effects in human and animals. However, our previous studies have shown that composite antimicrobial peptides (CAP) can have a protective effect in piglets challenged with DON. This study was conducted to evaluate the effect of the CAP GLAM 180# on the metabolism of piglets challenged with DON using a nuclear magnetic resonance (NMR)-based metabolomics approach. A total of 28 individually housed piglets (Duroc × Landrace × Large Yorkshire) weaned at 28 d of age were randomly assigned into 4 treatment groups (7 pigs/treatment) based on a 2 × 2 factorial arrangement that were fed, respectively, a basal diet (NC), basal diet + 0.4% CAP (basal + CAP), basal diet + 4 mg/kg DON (basal + DON), and basal diet + 4 mg/kg DON + 0.4% CAP (DON + CAP). A 7-d adaptation period was followed by 30 d of treatment. Blood samples were then collected for metabolite analysis by proton NMR (H-NMR) spectroscopy and liquid chromatography tandem mass spectrometry (LC-MS/MS). The combined results of H-NMR spectroscopy and LC-MS/MS showed that DON increased ( < 0.05) the serum concentrations of low-density lipoprotein, glycoprotein, urea, trimethylamine-N-oxide (TMAO), and lactate as well as those of almost all essential AA and some nonessential AA but decreased the concentrations of high-density lipoprotein (HDL), unsaturated lipids, citrate, choline, and fumarate compared with those in NC treatment ( < 0.05). There was a significant interaction effect ( < 0.05) of supplementation with DON and CAP on some metabolites showed that the serum concentrations of HDL, unsaturated lipids, Pro, citrate, and fumarate were greater ( < 0.05) whereas those of glycoprotein, urea, TMAO, Gly, and lactate were lower in the DON + CAP treatment compared with those in the basal + DON treatment ( < 0.05). These findings indicated that DON causes disturbances in AA, lipid, and energy metabolism and that CAP could partially attenuate the above metabolic disturbances induced by DON.

[Molecular candidates for capacitative calcium entry channel].

The emptying of intracellular calcium store generates a putative signal that induces the opening of the store-operated calcium channel (SOC) at the level of the cell membrane, also known as the capacitative calcium entry (CCE), or the calcium release-activated calcium channel (CRAC), which allows entry of calcium into the cells from the extracellular space. Drosophila transient receptor potential (trp) and trp-like(trpl) genes have been identified and reported to code cation channels(TRP and TRPL). The mechanism of coupling between store depletion and channel opening is unknown. Three fundamental mechanisms have been proposed for transmitting the signal from intracellular stores to the plasma membrane: (1) a diffusible message; (2) protein-protein interactions; and (3) vesicle secretion. This review focuses primarily on the recent studies on the TRP homologues, the possible mechanisms and electrophysiological phenotypes of capacitative calcium entry.