FAS Human ELISA Kit

Camelina and chia oils are among the vegetable oils (VOs) with high content of alpha-linolenic acid (ALA) and a combination of antioxidants, giving them nutritional advantage over other VOs used in aquafeeds. The present study evaluated the effects of dietary substitution of fish oil with oils from camelina or chia on the growth performance, fatty acid (FA) composition, gene expression and blood haematology in gilthead sea bream after a 90-day feeding trial. Five isoproteic and isolipidic diets were formulated in which fish oil was 100% (camelina oil, CSO diet; and chia oil, CO diet) or 60% (MIX1 and MIX2 diets containing camelina and chia oils, respectively) replaced with camelina or chia oils. Growth performance and FA profiles of fish were significantly affected by the dietary treatments (p < .05). Contents of eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and arachidonic acid (ARA) decreased, whereas n-3 polyunsaturated fatty acid (PUFA) and n-3/n-6 ratio increased in fish fed diets containing oils from camelina or chia. An up-regulation in the expression of genes involved in PUFA metabolism and the subsequent in vivo bioconversion of precursor FAs into highly unsaturated fatty acid (HUFA, C >= 20 andn >= 3) were recorded in fish fed VO-based diets. Red blood cells (RBC), white blood cells (WBC), haemoglobin and haematocrit did not differ among fish fed the experimental diets. Our overall results suggested that replacement of fish oil with camelina or chia oil did not adversely affect growth performance in gilthead sea bream, except for those fed CSO diet. Our results also demonstrate that fatty acid profile of fish can be modified by the dietary inclusion level of camelina or chia oils.

Osteoclasts are the principal mediators of bone resorption. They form through the fusion of mononuclear precursor cells under the principal influence of the cytokines macrophage colony stimulating factor (M-CSF, aka CSF-1) and receptor activator of NF-kappa B ligand (RANKL, aka TNFSF11). Sexual dimorphism in the development of the skeleton and in the incidence of skeletal diseases is well described. In general, females, at any given age, have a lower bone mass than males. The reasons for the differences in the bone mass of the skeleton between women and men at various ages, and the incidence of certain metabolic bone diseases, are multitude, and include the actions of sex steroids, genetics, age, environment and behavior. All of these influence the rate that osteoclasts form, resorb and die, and frequently produce different effects in females and males. Hence, a variety of factors are responsible for the sexual dimorphism of the skeleton and the activity of osteoclasts in bone. This review will provide an overview of what is currently known about these factors and their effects on osteoclasts.