Effect of arterially infused catecholamines and insulin on plasma glucose and free fatty acids in carp

Abstract

Common carp (Cyprinus carpio L.), kept at 20 degrees C, were fitted with an indwelling PE-50 cannula in the dorsal aorta. Hormones dissolved in Ringer saline were arterially infused at a rate of 1 microgram.kg-1.min-1 for epinephrine (Epi), 2 micrograms.kg-1.min-1 for norepinephrine (NE), and 1.33 micrograms.kg-1.min-1 for insulin. INfusion of bovine insulin in carp resulted in a long lasting (24 h) decrease of plasma free fatty acids (FFA; -0.41 +/- 0.06 mM) and glucose levels (-3.14 +/- 0.25 mM) compared with preinfusion levels at t = 0. Both Epi and NE induced a marked hyperglycemia although Epi was more potent (+8.2 +/- 0.9 and +6.9 +/- 0.8 mM, respectively). Plasma FFA levels increased by 0.25 +/- 0.03 mM compared with preinfusion levels on Epi infusion. In contrast, during NE infusion, plasma FFA levels decreased significantly by -0.21 +/- 0.03 mM. Plasma insulin titers did not significantly change during infusion of NE or Epi. It is concluded that the ratio of NE to Epi is the major factor that determines the effect of catecholamines on plasma FFA levels in carp. These results may explain species-dependent different effects of hypoxia on FFA metabolism in fish.

The stress response of the gilthead sea bream (Sparus aurata L.) to air exposure and confinement

“…Indeed, a similar increase in plasma -MSH concentrations was found in the short-term (24 h) confinement experiment, in which plasma cortisol concentrations already had returned to control values. As the -endorphin concentration was also increased in the long term, we do not exclude that synergistic effects of -MSH and -endorphin, as described for tilapia (Balm et al 1995), triggered the release of cortisol in long-term confined gilthead sea bream.…”

“…These results point to a sympathetic activation of the chromaffin cells in the head kidney and the release of catecholamines. Arterially infused catecholamines have been shown to induce hyperglycaemia in carp, and increased plasma lactate concentrations are associated with increased catecholamine concentrations and hypoxia (van Raaij et al 1995, 1996, Fabbri et al 1998. As gas exchange is compromised in air-exposed fish, the resulting hypoxia will contribute to the production of high lactate concentrations , Maxime et al 1995.…”

“…-melanocyte stimulating hormone ( -MSH), also has corticotrophic actions (Lamers et al 1992). Moreover, acetylated endorphins secreted by the -MSH cells have been suggested to potentiate the corticotrophic activity of -MSH (Balm et al 1995). Differential activation of the ACTH and the MSH cells have been reported in fish.…”

Effect of Sodium Chloride on Hematological and Biochemical Profile in Common Carp (Cyprinus carpio L.)

“…The hyperglycemia result from salinity stress is caused by catecholamines that affect the liver and release glucose from it (25). Also cortisol causes hyperglycemia by increased gluconeogenesis in peripheral tissue (26) .…”

Endocrine, Physiological and Histopathological Responses of Fish and their Larvae to Stress with Emphasis on Exposure to Crude Oil and Various Petroleum Hydrocarbons

“…Catecholamines stimulate glycogenolysis and gluconeogenesis, and consequently increase blood sugar providing an animal with a readily available energy source to deal with stressful conditions (Mazeaud and Mazeaud, 1981;Morata et al 1982;Ristori and Laurent, 1985;Suarez and Mommsen, 1987;Sheridan and Mur, 1988;Wright et al 1989;Pickering 1990;Wood et al 1990;Wendelaar Bonga, 1997). Adrenaline stimulates glycogenolysis by increasing levels of intracellular cyclic AMP, which then activates glycogen phosphorylase and causes the breakdown of glycogen to glucose (Morata et al 1982;Van Raaij et al 1995). There is also evidence to suggest the involvement of catecholamines in the mobilization of free fatty acids (Waring et al 1996b) though results are inconsistent (see review by Wendelaar Bonga, 1997) Catecholamines have a stimulatory action on cardiovascular function (Randall and Perry, 1992;Perry and Bernier, 1999), increasing heart rate (Wahlqvist and Nilsson, 1977;Satchell, 1991) stroke volume (Wood and Shelton, 1980;Mazeaud and Mazeaud, 1981;Pennec, 1987), blood pressure (Wahlqvist and Nilsson, 1977;Wood and Shelton, 1980) and branchial blood flow (Capra and Satchell, 1977;Butler and Metcalfe, 1983;Stagg and Shuttleworth, 1984).…”