Beta-adrenergic control of plasma glucose and free fatty acid levels in the air-breathing African catfish Clarias gariepinus Burchell 1822

In several water-breathing fish species, P-adrenergic receptor stimulation by noradrenaline leads to a decrease in plasma free fatty acid (FFA) levels, as opposed to an increase in air-breathing mammals. We hypothesised that this change in adrenergic control is related to the mode of breathing. Therefore, cannulated air-breathing African catfish were infused for 90 min with noradrenaline or with the nonselective P-agonist, isoprenaline. To identify the receptor type involved, a bolus of either a selective beta(1)-antagonist (atenolol) or a selective beta(2)-antagonist (ICI 118,551) was injected 15 min prior to the isoprenaline infusion. Both noradrenaline and isoprenaline led to an expected rise in glucose concentration. Isoprenaline combined with both the beta(1)- and beta(2)-antagonist led to higher glucose concentrations than isoprenaline alone. This could indicate the presence of a stimulatory P-adrenoceptor different from beta(1) and beta(2)-adrenoceptors; these two receptors thus seemed to mediate a reduction in plasma glucose concentration. Both noradrenaline and isoprenaline led to a significant decrease in FFA concentration. Whereas the beta(1)-antagonist had no effect, the beta(2)-antagonist reduced the decrease in FFA concentration, indicating the involvement of beta(2)-adrenoceptors. It is concluded that the air-breathing African catfish reflects water-breathing fish in the adrenergic control of plasma FFA and glucose levels

beta-adrenoceptors mediate inhibition of lipolysis in adipocytes of tilapia (Oreochromis mossambicus)

The regulation of triglyceride mobilization by catecholamines was investigated in the teleost fish Oreochromis mossambicus (tilapia) in vivo and in vitro. In vitro experiments were carried out with adipocytes that were isolated for the first time from fish adipose tissue. For the in vivo experiments, cannulated tilapia were exposed to stepwise decreasing oxygen levels (20, 10, and 5% air saturation; 3.9, 1.9, and 1.0 kPa PO2, respectively), each level being maintained for 2 h. Blood samples were taken at timed intervals and analyzed for plasma lactate, glucose, free fatty acids, epinephrine, norepinephrine, and cortisol. Hypoxia exposure did not change plasma epinephrine levels. In contrast, the plasma norepinephrine concentration markedly increased at all hypoxia levels. Over the same period, plasma free fatty acid levels showed a significant continuous decrease, suggesting that norepinephrine is responsible for the reduced plasma free fatty acid concentration, presumably through inhibition of lipolysis in adipose tissue. To elucidate the mechanism, adipocytes were isolated from mesenteric adipose tissue of tilapia and incubated with 1) norepinephrine, 2) norepinephrine + phentolamine (alpha(1),alpha(2)-antagonist), 3) isoproterenol (nonselective beta-agonist), 4) isoproterenol + timolol (beta(1),beta(2)-antagonist), 5) norepinephrine + timolol, and 6) BRL-35135A (beta(3)-agonist). The results demonstrate for the first time that norepinephrine and isoproterenol suppress lipolysis in isolated adipocytes of tilapia. The effect of norepinephrine is not mediated through alpha(2)-adrenoceptors but, like isoproterenol, via beta-adrenoceptors. Furthermore, this study provides strong indications that beta(3)-adrenoceptors are involved

Plasma lactate and stress hormones in common carp (Cyprinus carpio) and rainbow trout (Oncorhynchus mykiss) during stepwise decreasing oxygen levels

By measuring the lactate response it is possible to determine whether a teleost is able to adapt to a certain oxygen level. It is hypothesized that recovery will occur at oxygen levels above the critical oxygen level (PO2)(crit) reflected by a transient lactate increase. In contrast, continuous lactate accumulation occurs at oxygen levels below the (PO2)(crit), which will be lethal in case of prolonged exposure. Since catecholamines as well as cortisol increase the availability of glucose, it is expected that these stress hormones are involved in the activation of the anaerobic metabolism. Common carp and rainbow trout were cannulated and exposed to stepwise decreasing oxygen levels. At each oxygen level blood samples were taken at several time-points and analyzed for plasma lactate, adrenaline, noradrenaline and cortisol. The results show that both individual and inter-specific differences in lactate response occur during exposure to hypoxia. These differences can be associated with observed differences in behaviour. Whereas carp stayed quiet during the hypoxia treatment, trout displayed individually different behaviour. In contrast to the passive responders, the active responding trout did not survive as a result of continuous lactate accumulation. Interestingly, both in carp and trout a strong correlation exists between the lactate and catecholamine levels. This may indicate that these stress hormones are of importance for the metabolic changes occurring during anaerobic activation

Oxygen dependence of metabolism and cellular adaptation in vertebrate muscles: a review

The key roles the cardiovascular system play in the complex distribution of blood, and consequently oxygen, have been extensively studied in vertebrates. Numerous studies have also revealed the complex and varied ways in which tissues cope with compromised oxygen supply. The links between these two processes are the subject of much current research. This article aims to review how blood supply influences tissue oxygenation and affects metabolism, and how this might have played a role in the evolution of the complex muscle arrangements which characterise vertebrates. Muscle tissue is the greatest proportion of body mass in most vertebrates and undergoes dramatic alterations in metabolism and associated oxygen flux. Special attention is given to the myotome of fishes, in which the partitioning of the fibre types contrasts with the mosaic arrangement of tetrapods. This gives us the opportunity to study pure whole vascularised muscle blocks, rather than single fibres, and further explore the interrelationship between oxygen supply and tissue energetics.<br /

Effects of chronic exposure to lead, copper, zinc, and cadmium on biomarkers of the European eel, Anguilla anguilla

Exposure to specific metallic compounds can cause severe deleterious modifications in organisms. Fishes are particularly prone to toxic effects from exposure to metallic compounds via their environment. Species that inhabit estuaries or freshwater environments can be chronically affected by persistent exposure to a large number of metallic compounds, particularly those released by industrial activities. In this study, we exposed yellow eels (European eel, Anguilla anguilla) for 28 days to environmentally relevant concentrations of four specific metals; lead (300, 600, and 1,200 μg/l), copper (40, 120, and 360 μg/l), zinc (30, 60, and 120 μg/l) and cadmium (50, 150, and 450 μg/l). The selected endpoints to assess the toxicological effects were neurotransmission (cholinesterasic activity in nervous tissue), antioxidant defense, and phase II metabolism (glutathione-S-transferase [GST] activity, in both gills and liver tissues), and peroxidative damage. The results showed an overall lack of effects on acetylcholinesterase for all tested metals. Lead, copper, and cadmium exposure caused a significant, dose-dependent, increase in GST activity in gill tissue. However, liver GST only significantly increased following zinc exposure. No statistically significant effects were observed for the thiobarbituric acid reactive substances assay, indicating the absence of peroxidative damage. These findings suggest that, despite the occurrence of an oxidative-based response after exposure to lead, copper, and cadmium, this had no consequence in terms of peroxidative membrane damage; furthermore, cholinergic neurotoxicity caused by lead, copper, and cadmium did not occur. The implications of these results are further discussed