Corn gluten meal induces enteritis and decreases intestinal immunity and antioxidant capacity in turbot (Scophthalmus maximus) at high supplementation levels.

Corn gluten meal (CGM) is an important alternative protein source in aquafeed production. However, in turbot (Scophthalmus maximus), CGM could not be effectively utilized because of its low digestibility, the reason for which is still unclear. The purpose of the present study was to investigate and elucidate the cause for the poor utilization of CGM by turbot from the view of gut health. An 8-week feeding trial was conducted with turbot individuals (initial body weight 11.4 ± 0.2 g), which were fed with one of four isonitrogenous and isolipidic diets formulated to include 0%, 21.2%, 31.8%, and 42.6% CGM to progressively replace 0%, 33%, 50%, and 67% fish meal (FM) protein in a FM-based diet, respectively. The results showed that CGM caused dose-dependent decreases in (1) growth performance, nutrient digestibility, and feed utilization; (2) activities of brush-border membrane enzymes; (3) intestinal antioxidant indices of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase activities, and reduced glutathione level; (4) intestinal immune parameters of acid phosphatase activity, complement 3, complement 4, and IgM concentrations. Dose-dependent increases in the severity of the inflammation, with concomitant alterations on microvilli structure and increasing expression of inflammatory cytokine genes of Il-1ß, Il-8, and Tnf-α were observed but without a change in the intracellular junctions and the epithelial permeability established by the plasma diamine oxidase activity and D-lactate level examinations. In conclusion, the present work proved that CGM negatively affected the gut health of turbot by inducing enteritis and by decreasing intestinal immunity and antioxidant capacity, which could be one of the reasons for the reduced utilization of CGM by turbot.

Cytotoxic compounds generated in heated oil and assimilation of oil in Wistar rats.

We have previously suggested that gluten binds with decomposition products from thermally oxidized oil during frying, and that low-molecular-weight compounds bound to browned gluten damage the liver in rats. Ten-week-old male Wistar rats were fed for 11 weeks ad libitum a diet containing 7 wt% fresh frying oil and 0.1 wt% gluten heated in/without oil at 180 degrees C for 10 h. Feces collected weekly and serum were subjected to lipid and hematological analyses, respectively. Values obtained in the analyses did not differ from those of the control group. The results show that thermally processed gluten does not influence the digestion, absorption, metabolism, and growth of rats, regardless of the cytotoxic low-molecular-weight compounds, and that ingested fresh oil was assimilated normally. Together with the previous results, the odor of thermally processed gluten stimulated the rats' appetite, and completely assimilable fresh oil and cytotoxic low-molecular-weight compounds bound to gluten were ingested, and thus organ damage and rapid body weight increase were observed. As commercial deep-fried products are often made with repeatedly used oil with periodically added fresh oil, similar to the present experimental diet, obesity and organ damage may also occur in humans.