The interplay between nutrition and immune system is well recognised, however the true integration of research between nutrition, animal energy status and immune function is still far from clear. In fish nutrition, especially for species maintained in aquaculture, formulated feeds are significantly different from the natural diet with recent changes in nutrient sources, especially with protein and oil sources now being predominated by terrestrial derived ingredients. Additionally, many feeds are now incorporated to health management and termed functional feeds, which are believed to improve fish health, reduce disease outbreaks and/or improve post-infection recovery. Using new omics technologies, including transcriptomics (microarray and RNA-seq) and proteomics, the impacts of nutrition on the immune system is becoming clearer. By using molecular pathway enrichment analysis, modules of genes can indicate how both local (intestinal) and systemic immune function are being altered. Although great progress has been made to define the changes in host immune function, understanding the interplay between fish nutrition, intestinal microbiome and immune system is only just beginning to emerge.

Summary: Methionine restriction (MR) decreases body weight and adiposity and improves glucose homeostasis in rodents. Similar to caloric restriction,MRextends lifespan, but is accompanied by increased food intake and energy expenditure. Most studies have examinedMRin young animals; therefore, the aim of this study was to investigate the ability ofMRto reverse age‐induced obesity and insulin resistance in adult animals. Male C57BL/6J mice aged 2 and 12 months old were fedMR(0.172% methionine) or control diet (0.86% methionine) for 8 weeks or 48 h. Food intake and whole‐body physiology were assessed and serum/tissues analyzed biochemically. Methionine restriction in 12‐month‐old mice completely reversed age‐induced alterations in body weight, adiposity, physical activity, and glucose tolerance to the levels measured in healthy 2‐month‐old control‐fed mice. This was despite a significant increase in food intake in 12‐month‐oldMR‐fed mice. Methionine restriction decreased hepatic lipogenic gene expression and caused a remodeling of lipid metabolism in white adipose tissue, alongside increased insulin‐induced phosphorylation of the insulin receptor (IR) and Akt in peripheral tissues. Mice restricted of methionine exhibited increased circulating and hepatic gene expression levels ofFGF21, phosphorylation ofeIF2a, and expression ofATF4, with a concomitant decrease inIRE1α phosphorylation. Short‐term 48‐hMRtreatment increased hepaticFGF21 expression/secretion and insulin signaling and improved whole‐body glucose homeostasis without affecting body weight. Our findings suggest thatMRfeeding can reverse the negative effects of aging on body mass, adiposity, and insulin resistance through anFGF21 mechanism. These findings implicateMRdietary intervention as a viable therapy for age‐induced metabolic syndrome in adult humans.

The intestine, being a multifunctional organ central to both nutrient uptake, pathogen recognition and regulating the intestinal microbiome, has been subjected to intense research. This review will focus on the recent studies carried out using high-throughput gene expression approaches, such as microarray and RNA sequencing (RNA-seq). These techniques have advanced greatly in recent years, mainly as a result of the massive changes in sequencing methodologies. At the time of writing, there is a transition between relatively well characterised microarray platforms and the developing RNA-seq, with the prediction that within a few years as costs decrease and computation power increase, RNA-seq related approaches will supersede the microarrays. Comparisons between the approaches are made and specific examples of how the techniques have been used to examine intestinal responses to pathogens, dietary manipulations and osmoregulatory challenges are given.

Summary: Obesity results from prolonged imbalance of energy intake and energy expenditure. Animal models have provided a fundamental contribution to the historical development of understanding the basic parameters that regulate the components of our energy balance. Five different types of animal model have been employed in the study of the physiological and genetic basis of obesity. The first models reflect single gene mutations that have arisen spontaneously in rodent colonies and have subsequently been characterized. The second approach is to speed up the random mutation rate artificially by treating rodents with mutagens or exposing them to radiation. The third type of models are mice and rats where a specific gene has been disrupted or overexpressed as a deliberate act. Such genetically-engineered disruptions may be generated through the entire body for the entire life (global transgenic manipulations) or restricted in both time and to certain tissue or cell types. In all these genetically-engineered scenarios, there are two types of situation that lead to insights: where a specific gene hypothesized to play a role in the regulation of energy balance is targeted, and where a gene is disrupted for a different purpose, but the consequence is an unexpected obese or lean phenotype. A fourth group of animal models concern experiments where selective breeding has been utilized to derive strains of rodents that differ in their degree of fatness. Finally, studies have been made of other species including non-human primates and dogs. In addition to studies of the physiological and genetic basis of obesity, studies of animal models have also informed us about the environmental aspects of the condition. Studies in this context include exploring the responses of animals to high fat or high fat/high sugar (Cafeteria) diets, investigations of the effects of dietary restriction on body mass and fat loss, and studies of the impact of candidate pharmaceuticals on components of energy balance. Despite all this work, there are many gaps in our understanding of how body composition and energy storage are regulated, and a continuing need for the development of pharmaceuticals to treat obesity. Accordingly, reductions in the use of animal models, while ethically desirable, will not be feasible in the short to medium term, and indeed an expansion in activity using animal models is anticipated as the epidemic continues and spreads geographically.