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Singular or dual dietary depletions of vitamins C and E in Atlantic salmon parr increased susceptibility to Aeromonas salmonicida challenge. An array of immune parameters were evaluated to identify the involvement of these vitamin depletions on the immune response. Dietary vitamin E levels in salmon had no impact on haematological parameters, total serum protein or lysozyme levels. Similarly, dietary vitamin E levels did not affect leucocyte antibody production, macrophage activating factor (MAF) release and respiratory burst (RB) phenomena. However, haemolytic and opsonic properties of complement were compromised in vitamin E depleted salmon. Parenteral administration of vitamin E to vitamin E depleted carp did not elevate phytohaemagglutinin (PHA) lymphocyte proliferation responses or complement activity. In vitro additions of vitamin E to lymphocytes from carp fed a commercial diet did not elevate PHA proliferation responses either. The increased disease susceptibility provoked by dietary vitamin C restriction in Atlantic salmon was not correlated with serum protein levels, differential leucocyte numbers or phagocyte functions as tested by RB activity or phagocytosis by macrophages. Lymphocyte functions were operational in these fish as examined by MAF secretion and antibody production. Analogous to vitamin E depletion, dietary vitamin C restriction in salmon compromised complement haemolytic activity. Elevating the vitamin C content of diets above normal levels enhanced complement activity in salmon. Vitamin C was a potent modulator of rainbow trout leucocyte functions. In vitro supplementation of vitamin C in the sodium (NaAsc) or polyphosphate (PPAsc) form was required for PHA-proliferation responses. MAF secretion was also augmented by in vitro additions of NaAsc to leucocytes obtained from vitamin C depleted trout. Injecting NaAsc into depleted fish elevated PHA proliferation responses compared with saline-injected controls. Leucocytes from the latter group could recover proliferative responses to levels associated with NaAsc-injected fish with in vitro additions of 1x10-3 and 1x10-4M PPAsc. Increased disease susceptibility, reduced complement activity and haematocrit values were symptomatic of combined dietary vitamin C and E depletion in salmon parr. Total and differential leucocyte numbers, or serum parameters including antiprotease activity and total protein level were unaffected by this dietary regime. Although poorly adherent, macrophages obtained from dually depleted salmon had similar RB values and expressed greater responsiveness to a MAF-containing supernatant than vitamin sufficient counterparts. Lymphocyte functions were impervious to dual vitamin depletion as antibody and MAF production responses were intact. In vitro additions of NaAsc and PPAsc were shown to elevate RB responses in macrophages from vitamin-restricted and -adequate salmon. MAF secretion was demonstrated to be a temperature-dependent phenomenon in rainbow trout leucocytes. After 48h acclimation at low in vitro temperatures (6 C), leucocytes obtained from trout at 14C expressed impoverished MAF production. Acclimation of trout to 7 C did riot rescue MAF production. Also, normal RB activity was reduced in macrophages obtained from fish at 14 C after 48h at 6 C in vitro. However, if allowed to acclimate, these macrophages become more responsive to MAF and recovered RB activity to levels associated with macrophages held at 10 and 18C. RB responses of macrophages from fish at 7 C functioned equally well across a wide range of in vitro temperature regimes. Phagocytic activity of macrophages obtained from fish at 14 C and placed at 6 C in vitro for 48h expressed temperature sensitivity. This was especially apparent in fish fed a dietary ?-3/?-6 fatty acid ratio of 2.0. However, this dietary regime also elevated phagocytic activity of these macrophages to such an extent, that their response surpassed that of macrophages from fish fed commercial diets or ?-3/?-6 ratios of 0.5 and 1 even at low in vitro temperatures.

The causes of the ongoing metabolic disease pandemic are complex. Changes in human population genetics proceed slowly, so the recent increase in metabolic disease prevalence likely reflects environmental and behavioural changes. Our circadian (~ 24-hour) systems optimise our biology according to time of day. Artificial stimuli like electric lighting and around-the-clock food access enable waking behaviours, such as eating, at times at which our circadian systems prime us to sleep. Such mistimed behaviours may contribute to metabolic disease, as exemplified by increased risk of diabetes in shift workers. However, few researchers have concurrently explored associations between sleep, diet composition and timing, and metabolic health. Furthermore, many dietary analysis methods used have not been validated, precluding accurate inferences about diet-disease relationships. And few studies have assessed the metabolic effects of interventions to resynchronise the circadian system each day. I first helped validate myfood24, an online dietary recall tool, by completing all of the lab work for dietary protein and sugar biomarkers. myfood24 has comparable validity to the gold-standard recall method. Subsequent analysis of the myfood24 data showed that consuming calories later relative to sleep is associated with overweight and obesity. Next, analysis of a public database indicated that longer sleepers had lower body mass indices, smaller waists, and favourable blood lipid profiles. Finally, we assessed whether long-term supplementation of melatonin (a hormone that synchronises the circadian system) influences metabolic health, sleep, and diet in adults predisposed to diabetes. Contrary to our hypotheses, melatonin had few effects. This project helped validate myfood24, a tool that could unveil diet-disease relationships in future studies. These studies might have key public health implications. Our findings also strengthen the notions that mistimed eating and insufficient sleep contribute to obesity. Finally, this project shows that melatonin may not substantially influence metabolic health in relatively healthy adults.