In contrast, a high-protein diet enhanced renal IGF-1 levels only in normal rats, suggesting that the additional effects of a high-protein intake on compensatory renal hypertrophy are partially mediated by GH signaling.77 In fact, the renal anabolic effects of the high-protein diet are attenuated by the inhibition of the GH receptor.78 Particularly, protein and energy wasting (PEW) is commonly observed in hemodialysis patients and likely associated with a lower protein and caloric intake.79 In this respect, circulating IGF-1 has been well-established as a marker for nutritional deficiency in hemodialysis patients for decades.80,81 Thus, patients undergoing hemodialysis with decreased muscle mass and a history of infections often show decreased serum IGF-1 levels, showing high sensitivity (77%) and moderate specificity (52%) as a marker of nutritional status.82 Compared to controls on a low-protein diet, rats fed a high-protein diet showed increased IGF-1 levels in the serum, liver and glomerulus, but not in the renal cortex, which resulted in higher total body and kidney weight but not liver
Increases in the concentrations of long- and very-long-chain fatty acids, suggesting their impaired -oxidation, were reported in the serum of ASD children [13,14]
Mitochondria, as the core source and main target of ROS [449], their functional damage will further form a positive feedback loop of ROS generation - mitochondrial damage, causing energy metabolism disorders and inducing mitochondria to release pro-apoptotic factors such as cytochrome C, ultimately leading to neuronal apoptosis [450]
FDG uptake and glucose transporter subtype expressions in experimental tumor and inflammation models
