Stress-induced effects on feeding behavior and growth performance of the sea bass (Dicentrarchus labrax): a self-feeding approach

Abstract

Repetitive aquaculture-related protocols may act as cyclic stressors that induce chronic stress in cultured fish. The sea bass is particularly sensitive to stressful conditions and the mere presence of humans will disturb feeding behavior. In this paper, we study whether chronic stress induced by repetition of acute stress protocols affects long-term feeding behavior and growth performance in sea bass and whether exogenous cortisol may induce stress-like changes in these parameters. We demonstrate that both chronic stress and dietary cortisol decrease food intake and have a negative effect on feed conversion efficiency, severely impairing sea bass performance. Both experimental approaches induced changes in the daily feeding activity by lengthening the active feeding periods. Fish subjected to a cyclic stressor modify their daily feeding pattern in an attempt to avoid interference with the time of the stressor. The delay in feeding when fish are acutely and repeatedly stressed could be of substantial adaptive importance.

Prenatal stress from trawl capture affects mothers and neonates: a case study using the southern fiddler ray (Trygonorrhina dumerilii)

“…We think that a connection between feeding and G:L ratio is likely because of the more general effects of nutritional state on immunocompetence4344, and under nutrient-limited conditions during reproduction immune function can be impaired31. Although we did not quantify food intake, the mass change in trawled females was consistent with the reduced appetite and food intake seen in teleost species subjected to acute stress45464748. Therefore, an increased strain on energetic resources allocated to both immune and reproductive functions may have also contributed to the reduction in maternal post-partum BM that we measured.…”

Chronic cortisol and the regulation of food intake and the endocrine growth axis in rainbow trout

“…Similarly, chronic plasma cortisol elevations have previously been shown to suppress feeding in rainbow trout (Gregory & Wood 1999), channel catfish (Peterson & Small 2005) and sea bass (Dicentrarchus labrax; Leal et al 2011), although the cortisol dosages used in these studies resulted in plasma cortisol levels that were at least two-times higher than those of the Cort-II treatment. In goldfish, chronic treatment with high plasma cortisol levels (w270 ng/ml) also inhibited food intake, but lower levels (w50 ng/ml) had a stimulatory effect Bernier et al 2004).…”

“…Bernier et al 2004, Peterson & Small 2005, Leal et al 2011 showing that chronically elevated cortisol levels inhibit growth. In addition, our results demonstrate that the factors contributing to the growth-suppressing effects of cortisol are differentially recruited according to plasma cortisol levels.…”

“…While the primary effect of glucocorticoids in mammals and amphibians is to increase food intake (Crespi et al 2004, Bazhan & Zelena 2013, the actions of cortisol on appetite in fish are equivocal. Whereas chronic exposure to a low dose of cortisol stimulated food intake in goldfish (Carassius auratus; Bernier et al 2004), sustained exposure to higher doses of cortisol decreased food intake in several fish species (Gregory & Wood 1999, Bernier et al 2004, Peterson & Small 2005, Leal et al 2011. In mammals, glucocorticoids promote food intake by stimulating the hypothalamic expression of the orexigenic neuropeptides neuropeptide Y (NPY) and agouti-related peptide (AgRP), and by inhibiting the anorexigenic signal corticotropinreleasing factor (CRF; Bazhan & Zelena 2013).…”

“…Similarly, the stimulatory effects of cortisol on food intake in goldfish are associated with an increase in hypothalamic NPY mRNA levels and a reduction in preoptic area (POA) CRF gene expression (Bernier et al 2004). In contrast, the pathways mediating the anorexigenic effects of cortisol in fish have yet to be identified (Bernier et al 2004, Leal et al 2011. In mammals, glucocorticoids are a potent stimulator of adipocyte leptin expression and secretion, and under conditions of glucocorticoid excess leptin can counteract the orexigenic effects of cortisol (Leal-Cerro et al 2001, Lee & Fried 2009).…”