+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Tissue-Specific Orchestration of Gilthead Sea Bream Resilience to Hypoxia and High Stocking Density


      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Two different O 2 levels (normoxia: 75–85% O 2 saturation; moderate hypoxia: 42–43% O 2 saturation) and stocking densities (LD: 9.5, and HD: 19 kg/m 3) were assessed on gilthead sea bream ( Sparus aurata) in a 3-week feeding trial. Reduced O 2 availability had a negative impact on feed intake and growth rates, which was exacerbated by HD despite of the improvement in feed efficiency. Blood physiological hallmarks disclosed the enhancement in O 2-carrying capacity in fish maintained under moderate hypoxia. This feature was related to a hypo-metabolic state to cope with a chronic and widespread environmental O 2 reduction, which was accompanied by a differential regulation of circulating cortisol and growth hormone levels. Customized PCR-arrays were used for the simultaneous gene expression profiling of 34–44 selected stress and metabolic markers in liver, white skeletal muscle, heart, and blood cells. The number of differentially expressed genes ranged between 22 and 19 in liver, heart, and white skeletal muscle to 5 in total blood cells. Partial Least-Squares Discriminant Analysis (PLS-DA) explained [R2Y(cum)] and predicted [Q2Y(cum)] up to 95 and 65% of total variance, respectively. The first component (R2Y = 0.2889) gathered fish on the basis of O 2 availability, and liver and cardiac genes on the category of energy sensing and oxidative metabolism ( cs, hif-1α, pgc1α, pgc1β, sirts 1- 2- 4- 5- 6- 7), antioxidant defense and tissue repair ( prdx5, sod2, mortalin, gpx4, gr, grp-170, and prdx3) and oxidative phosphorylation ( nd2, nd5, and coxi) highly contributed to this separation. The second component (R2Y = 0.2927) differentiated normoxic fish at different stocking densities, and the white muscle clearly promoted this separation by a high over-representation of genes related to GH/IGF system ( ghr-i, igfbp6b, igfbp5b, insr, igfbp3, and igf-i). The third component (R2Y = 0.2542) discriminated the effect of stocking density in fish exposed to moderate hypoxia by means of hepatic fatty acid desaturases ( fads2, scd1a, and scd1b) and muscle markers of fatty acid oxidation ( cpt1a). All these findings disclose the different contribution of analyzed tissues (liver ≥ heart > muscle > blood) and specific genes to the hypoxic- and crowding stress-mediated responses. This study will contribute to better explain and understand the different stress resilience of farmed fish across individuals and species.

          Related collections

          Most cited references87

          • Record: found
          • Abstract: found
          • Article: not found

          Ecophysiology. Climate change tightens a metabolic constraint on marine habitats.

          Warming of the oceans and consequent loss of dissolved oxygen (O2) will alter marine ecosystems, but a mechanistic framework to predict the impact of multiple stressors on viable habitat is lacking. Here, we integrate physiological, climatic, and biogeographic data to calibrate and then map a key metabolic index-the ratio of O2 supply to resting metabolic O2 demand-across geographic ranges of several marine ectotherms. These species differ in thermal and hypoxic tolerances, but their contemporary distributions are all bounded at the equatorward edge by a minimum metabolic index of ~2 to 5, indicative of a critical energetic requirement for organismal activity. The combined effects of warming and O2 loss this century are projected to reduce the upper ocean's metabolic index by ~20% globally and by ~50% in northern high-latitude regions, forcing poleward and vertical contraction of metabolically viable habitats and species ranges.
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            Triglycerides Promote Lipid Homeostasis during Hypoxic Stress by Balancing Fatty Acid Saturation

            Summary Lipid droplets, which store triglycerides and cholesterol esters, are a prominent feature of clear cell renal cell carcinoma (ccRCC). Although their presence in ccRCC is critical for sustained tumorigenesis, their contribution to lipid homeostasis and tumor cell viability is incompletely understood. Here we show that disrupting triglyceride synthesis compromises the growth of both ccRCC tumors and ccRCC cells exposed to tumor-like conditions. Functionally, hypoxia leads to increased fatty acid saturation through inhibition of the oxygen-dependent stearoyl-CoA desaturase (SCD) enzyme. Triglycerides counter a toxic buildup of saturated lipids, primarily by releasing the unsaturated fatty acid oleate (the principal product of SCD activity) from lipid droplets into phospholipid pools. Disrupting this process derails lipid homeostasis, causing overproduction of toxic saturated ceramides and acyl-carnitines as well as activation of the NF-κB transcription factor. Our work demonstrates that triglycerides promote homeostasis by “buffering” specific fatty acids.
              • Record: found
              • Abstract: found
              • Article: not found

              Insulin stimulates hypoxia-inducible factor 1 through a phosphatidylinositol 3-kinase/target of rapamycin-dependent signaling pathway.

              Hypoxia-inducible factor 1 (HIF-1) is a transcription factor involved in normal mammalian development and in the pathogenesis of several disease states. It consists of two subunits, HIF-1alpha, which is degraded during normoxia, and HIF-1beta, which is constitutively expressed. Activated HIF-1 induces the expression of genes involved in angiogenesis, erythropoiesis, and glucose metabolism. We have previously reported that insulin stimulates vascular endothelial growth factor (VEGF) expression (). In this study, we show that insulin activates HIF-1, leading to VEGF expression in retinal epithelial cells. Insulin activates HIF-1alpha protein expression in a dose-dependent manner with a maximum reached within 6 h. The expression of HIF-1alpha is correlated with the activation of HIF-1 DNA binding activity and the transactivation of a HIF-1-dependent reporter gene. Insulin does not appear to affect HIF-1alpha mRNA transcription but regulates HIF-1alpha protein expression through a translation-dependent pathway. The expression of an active form of protein kinase B and treatment of cells with specific inhibitors of phosphatidylinositol 3-kinase (PI3K), MAPK, and target of rapamycin (TOR) show that mainly PI3K and to a lesser extent TOR are required for insulin-induced HIF-1alpha expression. HIF-1 activity and VEGF expression are also dependent on PI3K- and TOR-dependent signaling. In conclusion, we show here that insulin regulates HIF-1 action through a PI3K/TOR-dependent pathway, resulting in increased VEGF expression.

                Author and article information

                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                10 July 2019
                : 10
                : 840
                Nutrigenomics and Fish Growth Endocrinology, Institute of Aquaculture Torre de la Sal (IATS-CSIC) , Castellón, Spain
                Author notes

                Edited by: José Luis Soengas, University of Vigo, Spain

                Reviewed by: Ivan Viegas, University of Coimbra, Portugal; Lluis Tort, Autonomous University of Barcelona, Spain

                †Present address: Juan Antonio Martos-Sitcha, Department of Biology, Faculty of Marine and Environmental Sciences, Instituto Universitario de Investigación Marina (INMAR), Campus de Excelencia Internacional del Mar (CEI-MAR), University of Cádiz, Cádiz, Spain Verónica de las Heras, Futuna Blue España S.L., El Puerto de Santa María, Cádiz, Spain

                This article was submitted to Aquatic Physiology, a section of the journal Frontiers in Physiology

                Copyright © 2019 Martos-Sitcha, Simó-Mirabet, de las Heras, Calduch-Giner and Pérez-Sánchez.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                : 01 January 2019
                : 19 June 2019
                Page count
                Figures: 4, Tables: 3, Equations: 0, References: 115, Pages: 18, Words: 0
                Funded by: Horizon 2020 Framework Programme 10.13039/100010661
                Award ID: AQUAEXCEL2020 (652831)
                Funded by: Ministerio de Economía y Competitividad 10.13039/501100003329
                Award ID: Juan de la Cierva-Formación, Reference FJCI-2014-20161
                Original Research

                Anatomy & Physiology
                hematology,hypometabolism,hypoxia,limiting oxygen saturation,sparus aurata,stocking density,tissue-specific transcriptomics


                Comment on this article