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It has been suggested that the removal of infected viscera on board is responsible for the high prevalence of anisakid larvae present in wild fish species. The aim of this work is to assess the re-infection capacity of anisakid larvae in European seabasses, a natural host species for the parasite by feeding with pieces of parasitised hake liver under controlled experimental conditions.To prove this potential link between manipulation and re-infestation, 50 farmed seabasses free of anisakid nematodes were fed with fresh hake liver pieces naturally infested with anisakid larvae.After digestion periods from 4 to 21 days, the seabasses showed a prevalence of Anisakis of 6%, and a low retention rate of 0.11 larvae/seabass after four days' digestion, and 0.0021 after 21 day digestion. Two nematodes were found in the intestine and in the visceral cavity, and 13 Anisakis were found partially digested in the stomach of one same individual after 4 day digestion. Results showed that only a small number of Anisakis ingested with the viscera were able to reinfect the seabasses, as most of the larvae seemed to be quickly digested or defecated.it seems that the availability of larvae that could re-enter the life cycle and re-infect a fish after the removal and discarding the infected viscera on board could be much less important than commonly believed.

We analysed the spatial and temporal variability of Anisakis larvae infection in hake (Merluccius merluccius) from the North-East Atlantic from 1998 to 2020 and the potential drivers (i.e., environmental and host abundance) of such variation. The results showed that hake from separate sea areas in the North Atlantic have marked differences in temporal abundance levels. Hake larger than 60 cm were all parasitized in all ICES (International Council for the Exploration of the Sea) subareas 6, 7, and 8. The belly flaps were the most parasitized parts of the flesh, accounting for 92% of the total. Individuals of Anisakis simplex, Anisakis pegreffii, Anisakis spp. and a hybrid of Anisakis simplex × pegreffii were genetically identified, and Anisakis simplex as the most abundant (88-100%). An ecological niche model of Anisakis occurrence in fishes in the NE Atlantic was built to define the thermal optimum and environmental ranges for salinity, depth, chlorophyll concentration, and diffuse attenuation. The temporal variability of anisakid infection in fishes in the last two decades indicated an increase in the NE Atlantic at an annual rate of 31.7 nematodes per total number of specimens examined per year. This rise in infection levels could be triggered by the increase in intermediate host fish stocks, especially hake in the area.

Studies conducted in mice have revealed positive effects of punicic acid (PUA). The aim of this study was to analyze the effects of PUA on fat accumulation and glycemic control in rats fed an obesogenic diet. Rats were randomly divided into two groups: control group and PUA group (diet supplemented with 0.5% PUA). No changes were observed in adipose tissue weights. The glucose tolerance test showed that the glycemic value in the PUA group had decreased significantly at the final time (120 min) (-19.3%), as had fructosamine levels (-11.1%). However, homeostasis model assessment (HOMA-IR) showed that insulin resistance did not improve. No changes were observed in the liver, skeletal muscle composition, or peroxisome proliferator-activated receptors (PPARs) activation. Low levels (mg/g tissue) of PUA (0.04 ± 0.01 in both tissues) and higher levels of cis-9,trans-11 conjugated linoleic acid (0.31 ± 0.08 in liver, 0.52 ± 0.11 in muscle) were found. PUA supplementation induced hypoplasia (-16.1%) due to the antiproliferative effect on hepatocytes. In conclusion, dietary supplementation of 0.5% PUA did not lead to decreased fat accumulation in adipose tissue, liver, or skeletal muscle, or to improved glycemic control. The hypoplasia induced in liver is a negative effect that should be considered before proposing PUA as a functional ingredient.