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, beta-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 beta-agonist, isoprenaline. To identify the receptor type involved, a bolus of either a selective beta1-antagonist (atenolol) or a selective beta2-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 beta1- and beta2-antagonist led to higher glucose concentrations than isoprenaline alone. This could indicate the presence of a stimulatory beta-adrenoceptor different from beta1 and beta2-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 beta1-antagonist had no effect, the beta2-antagonist reduced the decrease in FFA concentration, indicating the involvement of beta2-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 PO(2), 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.