Short‐term metabolic responses of gilthead seabream, Sparus aurata , fed diets with different protein and protein: Energy levels

2021 ◽  
Author(s):  
Renan Rosa Paulino ◽  
Alexandre Firmino Diógenes ◽  
Kátia Rodrigues Batista Oliveira ◽  
Tamira Maria Orlando ◽  
Priscila Vieira Rosa ◽  
...  
2020 ◽  
Vol 11 ◽  
Author(s):  
Lourenço Ramos-Pinto ◽  
Rita Azeredo ◽  
Carlota Silva ◽  
Luís E. C. Conceição ◽  
Jorge Dias ◽  
...  

2014 ◽  
Vol 155 ◽  
pp. 101-108 ◽  
Author(s):  
Marcelino Herrera ◽  
Maria Filipa Castanheira ◽  
Luis E.C. Conceição ◽  
Catarina I. Martins

Animals ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 3310
Author(s):  
Jorge Aedo ◽  
Daniela Aravena-Canales ◽  
Ignacio Ruiz-Jarabo ◽  
Ricardo Oyarzún ◽  
Alfredo Molina ◽  
...  

Cortisol is the main glucocorticoid hormone promoting compensatory metabolic responses of stress in teleosts. This hormone acts through genomic and membrane-initiated actions to exert its functions inside the cell. Experimental approaches, using exogenous cortisol administration, confirm the role of this hormone during short (minutes to hours)- and long-term (days to weeks) responses to stress. The role of membrane-initiated cortisol signaling during long-term responses has been recently explored. In this study, Sparus aurata were intraperitoneally injected with coconut oil alone or coconut oil containing cortisol, cortisol-BSA, or BSA. After 3 days of treatment, plasma, liver, and skeletal muscle were extracted. Plasma cortisol, as well as metabolic indicators in the plasma and tissues collected, and metabolism-related gene expression, were measured. Our results showed that artificially increased plasma cortisol levels in S. aurata enhanced plasma glucose and triacylglycerols values as well as hepatic substrate energy mobilization. Additionally, cortisol stimulated hepatic carbohydrates metabolism, as seen by the increased expression of metabolism-related genes. All of these responses, observed in cortisol-administered fish, were not detected by replicating the same protocol and instead using cortisol-BSA, which exclusively induces membrane-initiated effects. Therefore, we suggest that after three days of cortisol administration, only genomic actions are involved in the metabolic responses in S. aurata.


2019 ◽  
Vol 91 ◽  
pp. 391
Author(s):  
L. Ramos-Pinto ◽  
C. Silva ◽  
R. Azeredo ◽  
L.E.C. Conceição ◽  
J. Dias ◽  
...  

Aquaculture ◽  
2021 ◽  
Vol 537 ◽  
pp. 736462
Author(s):  
I. Elalfy ◽  
H.S. Shin ◽  
D. Negrín-Báez ◽  
A. Navarro ◽  
M.J. Zamorano ◽  
...  

2021 ◽  
Author(s):  
José Carlos Campos‐Sánchez ◽  
Francisco A. Guardiola ◽  
José María García Beltrán ◽  
Diana Ceballos‐Francisco ◽  
María Ángeles Esteban

Animals ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 753
Author(s):  
Andre Barany ◽  
Juan Fuentes ◽  
Gonzalo Martínez-Rodríguez ◽  
Juan Miguel Mancera

Several studies in fish have shown that aflatoxin B1 (AFB1) causes a disparity of species-dependent physiological disorders without compromising survival. We studied the effect of dietary administration of AFB1 (2 mg AFB1 kg−1 diet) in gilthead seabream (Sparus aurata) juveniles in combination with a challenge by stocking density (4 vs. 40 g L−1). The experimental period duration was ten days, and the diet with AFB1 was administered to the fish for 85 days prior to the stocking density challenge. Our results indicated an alteration in the carbohydrate and lipid metabolites mobilization in the AFB1 fed group, which was intensified at high stocking density (HSD). The CT group at HSD increased plasma cortisol levels, as expected, whereas the AFB1-HSD group did not. The star mRNA expression, an enzyme involved in cortisol synthesis in the head kidney, presented a ninefold increase in the AFB1 group at low stocking density (LSD) compared to the CT-LSD group. Adenohypophyseal gh mRNA expression increased in the AFB1-HSD but not in the CT-HSD group. Overall, these results confirmed that chronic AFB1 dietary exposure alters the adequate endocrinological physiological cascade response in S. aurata, compromising the expected stress response to an additional stressor, such as overcrowding.


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