In our study, a concomitant increase in ROS production, the down regulation of the antioxidant enzymes activities and a change of lipid peroxidation were crucial for the onset of cell death.
A hypothesis to account for the change of lipid granules would be that PQBP1 regulates expression of Fsp27/CIDE-C, which locates at lipid droplets and influences their size [23], like PPAR-γ regulates Fsp27 [24].
In this context, it is interesting to note that some peptides implicated in fat metabolism were conspicuously absent in the non-diapausing larvae of Nasonia [Figure 1 and supplementary table S1], which further corroborates a change of lipid metabolism with diapause in Nasonia.
However, these studies only determined the change of lipid metabolism related genes expression and enzyme activities after dietary Cu treatment.
Generally, the change of lipid involves only a small Δρo, excepting the case of WGWALP23 (see below) and the highly dynamic YGWALP23, noted previously.
To shed light on the molecular mechanisms underlying the change of lipid storage in yellow catfish, we analyzed the changes of mRNA expression of these ER-related genes known to play an important molecular role in ER stress induced changes of lipid deposition.
Thus, considering the important role ER plays in lipid metabolism, we hypothesize that ER stress dependent alteration in lipid homeostasis was the mechanism that underlies the change of lipid deposition of yellow catfish in responses to dietary copper levels.
Accordingly, creatine supplementation has been associated with either no change of lipid peroxidation, resistance of low density lipoprotein to oxidative stress or plasma concentrations of nonenzymatic antioxidants [ 39], increased free radical generation [ 37], and reduced oxidative stress [ 38].
Unpaired Student's t-tests were performed for comparisons of differences in the relative change of lipid levels and serum TNF-α levels at 4 weeks and 24 weeks between ETA + MTX and MTX as monotherapy groups.
There is now a large body of evidence indicating that this change of lipid profile is favorable in relation to atherosclerosis and CVD, and this diet therefore is likely to be antiatherogenic also in RA.
