scholarly journals Nutritional regulation of glucose-6-phosphatase gene expression in liver of the gilthead sea bream (Sparus aurata)

2002 ◽  
Vol 88 (6) ◽  
pp. 607-614 ◽  
Author(s):  
A. Caseras ◽  
I. Metón ◽  
C. Vives ◽  
M. Egea ◽  
F. Fernández ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Sparus Aurata ◽  
Gilthead Sea Bream ◽  
Sea Bream ◽  
Metabolic Adaptation ◽  
Mrna Levels ◽  
Nutritional Regulation ◽  
Carnivorous Fish ◽  
Hepatic Expression ◽  
Glucose Levels

To examine the role of glucose-6-phosphatase (G6Pase) in glucose homeostasis in the diabetes-like experimental model of carnivorous fish, we analysed postprandial variations and the effect of starvation, ration size and diet composition on the regulation of G6Pase expression at the enzyme activity and mRNA level in the liver of gilthead sea bream (Sparus aurata). G6Pase expression increased in long-term starved or energy-restricted fish. In contrast to data reported for other fish species, short-term regulation of G6Pase expression was found in regularly fedS. aurata. G6Pase mRNA levels were lowest between 4 and 15 h after food intake, whereas minimal enzyme activity was observed 10–15 h postprandially. Alterations of plasma glucose levels affect G6Pase in mammals. However, the carbohydrate content of the diet did not affect hepatic expression of G6Pase inS. aurata, suggesting that a different molecular mechanism is involved in the control of G6Pase expression in fish. Although G6Pase was unaffected, high-carbohydrate low-protein diets increased glucokinase (GK) expression and thus allowed a metabolic adaptation favouring glycolysis over gluconeogenesis. Interestingly, only the nutritional conditions that promoted variations in the blood glucose levels resulted in changes in the hepatic expression of G6Pase. These findings indicate a concerted regulation of G6Pase and GK expression and suggest that the direction and rate of the glucose–glucose-6-phosphate substrate cycle flux is finely regulated in the liver ofS. aurata, challenging the role attributed to deficient regulation of G6Pase or GK expression in the low ability of carnivorous fish to metabolize glucose.

scholarly journals Specific Evolution and Gene Family Expansion of Complement 3 and Regulatory Factor H in Fish

2020 ◽  
Vol 11 ◽  
Author(s):  
Babak Najafpour ◽  
João C. R. Cardoso ◽  
Adelino V. M. Canário ◽  
Deborah M. Power
Keyword(s):  
Complement System ◽  
Sparus Aurata ◽  
Factor H ◽  
Gilthead Sea Bream ◽  
Sea Bream ◽  
Immune Gene ◽  
Gene Repertoire ◽  
Tandem Gene Duplication ◽  
Hepatic Expression ◽  
The Complement System

The complement system comprises a large family of plasma proteins that play a central role in innate and adaptive immunity. To better understand the evolution of the complement system in vertebrates and the contribution of complement to fish immunity comprehensive in silico and expression analysis of the gene repertoire was made. Particular attention was given to C3 and the evolutionary related proteins C4 and C5 and to one of the main regulatory factors of C3b, factor H (Cfh). Phylogenetic and gene linkage analysis confirmed the standing hypothesis that the ancestral c3/c4/c5 gene duplicated early. The duplication of C3 (C3.1 and C3.2) and C4 (C4.1 and C4.2) was likely a consequence of the (1R and 2R) genome tetraploidization events at the origin of the vertebrates. In fish, gene number was not conserved and multiple c3 and cfh sequence related genes were encountered, and phylogenetic analysis of each gene generated two main clusters. Duplication of c3 and cfh genes occurred across the teleosts in a species-specific manner. In common, with other immune gene families the c3 gene expansion in fish emerged through a process of tandem gene duplication. Gilthead sea bream (Sparus aurata), had nine c3 gene transcripts highly expressed in liver although as reported in other fish, extra-hepatic expression also occurs. Differences in the sequence and protein domains of the nine deduced C3 proteins in the gilthead sea bream and the presence of specific cysteine and N-glycosylation residues within each isoform was indicative of functional diversity associated with structure. The diversity of C3 and other complement proteins as well as Cfh in teleosts suggests they may have an enhanced capacity to activate complement through direct interaction of C3 isoforms with pathogenic agents.

scholarly journals Metformin counteracts glucose-dependent lipogenesis and impairs transdeamination in the liver of gilthead sea bream (Sparus aurata)

2019 ◽  
Vol 316 (3) ◽  
pp. R265-R273 ◽  
Author(s):  
Ania Rashidpour ◽  
Jonás I. Silva-Marrero ◽  
Lidia Seguí ◽  
Isabel V. Baanante ◽  
Isidoro Metón
Keyword(s):  
Molecular Mechanisms ◽  
Sparus Aurata ◽  
Current Knowledge ◽  
Tricarboxylic Acid Cycle ◽  
Intraperitoneal Administration ◽  
Metabolic Effects ◽  
Gilthead Sea Bream ◽  
Sea Bream ◽  
Glucose Load ◽  
Carnivorous Fish

Metformin is an antidiabetic drug with a major impact on regulating blood glucose levels by decreasing hepatic gluconeogenesis, but also by affecting other pathways, including glucose transport and energy/lipid metabolism. Carnivorous fish are considered glucose intolerant, as they exhibit poor ability in using dietary carbohydrates. To increase the current knowledge about the molecular mechanisms by which metformin can improve glucose homeostasis in carnivorous fish, we addressed the effect of intraperitoneal administration of metformin, in the presence or absence of a glucose load, on metabolic rate-limiting enzymes and lipogenic factors in the liver of gilthead sea bream ( Sparus aurata). Hyperglycemia markedly upregulated the expression of glycolytic enzymes (glucokinase and 6-phosphofructo-1-kinase, PFK1) 5 h following glucose administration, while at 24 h posttreatment, it increased isocitrate dehydrogenase (IDH) activity, a key enzyme of the tricarboxylic acid cycle, and the expression of lipogenic factors (PGC1β, Lpin1, and SREBP1). Metformin counteracted glucose-dependent effects, and downregulated glutamate dehydrogenase, alanine aminotransferase, and mammalian target of rapamycin 5 h posttreatment in the absence of a glucose load, leading to decreased long-term activity of PFK1 and IDH. The results of the present study suggest that hyperglycemia enhances lipogenesis in the liver of S. aurata and that metformin may exert specific metabolic effects in fish by decreasing hepatic transdeamination and suppressing the use of amino acids as gluconeogenic substrates. Our findings highlight the role of amino acid metabolism in the glucose-intolerant carnivorous fish model.

scholarly journals Diet and Exercise Modulate GH-IGFs Axis, Proteolytic Markers and Myogenic Regulatory Factors in Juveniles of Gilthead Sea Bream (Sparus aurata)

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2182
Author(s):  
Miquel Perelló-Amorós ◽  
Isabel García-Pérez ◽  
Albert Sánchez-Moya ◽  
Arnau Innamorati ◽  
Emilio J. Vélez ◽  
...  
Keyword(s):  
Sparus Aurata ◽  
High Energy ◽  
Culture Conditions ◽  
Gilthead Sea Bream ◽  
Sea Bream ◽  
Mrna Levels ◽  
Myogenic Regulatory Factors ◽  
Regulatory Factors ◽  
Gene And Protein Expression ◽  
Plasma Gh

The physiological and endocrine benefits of sustained exercise in fish were largely demonstrated, and this work examines how the swimming activity can modify the effects of two diets (high-protein, HP: 54% proteins, 15% lipids; high-energy, HE: 50% proteins, 20% lipids) on different growth performance markers in gilthead sea bream juveniles. After 6 weeks of experimentation, fish under voluntary swimming and fed with HP showed significantly higher circulating growth hormone (GH) levels and plasma GH/insulin-like growth-1 (IGF-1) ratio than fish fed with HE, but under exercise, differences disappeared. The transcriptional profile of the GH-IGFs axis molecules and myogenic regulatory factors in liver and muscle was barely affected by diet and swimming conditions. Under voluntary swimming, fish fed with HE showed significantly increased mRNA levels of capn1, capn2, capn3, capns1a, n3, and ub, decreased gene and protein expression of Ctsl and Mafbx and lower muscle texture than fish fed with HP. When fish were exposed to sustained exercise, diet-induced differences in proteases’ expression and muscle texture almost disappeared. Overall, these results suggest that exercise might be a useful tool to minimize nutrient imbalances and that proteolytic genes could be good markers of the culture conditions and dietary treatments in fish.

scholarly journals Sterol Regulatory Element Binding Protein-1a Transactivates 6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase Gene Promoter

Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3446-3456 ◽  
Author(s):  
Isidoro Metón ◽  
Miriam Egea ◽  
Ida G. Anemaet ◽  
Felipe Fernández ◽  
Isabel V. Baanante
Keyword(s):  
Transcriptional Activation ◽  
Sparus Aurata ◽  
Binding Protein ◽  
Regulatory Element ◽  
Gene Promoter ◽  
Sea Bream ◽  
Proximal Promoter ◽  
Mrna Levels ◽  
Nutritional Regulation ◽  
Sterol Regulatory Element

6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB) catalyzes the synthesis and degradation of fructose-2,6-bisphosphate, a key modulator of glycolysis-gluconeogenesis. To gain insight into the molecular mechanism behind hormonal and nutritional regulation of PFKFB expression, we have cloned and characterized the proximal promoter region of the liver isoform of PFKFB (PFKFB1) from gilthead sea bream (Sparus aurata). Transient transfection of HepG2 cells with deleted gene promoter constructs and electrophoretic mobility shift assays allowed us to identify a sterol regulatory element (SRE) to which SRE binding protein-1a (SREBP-1a) binds and transactivates PFKFB1 gene transcription. Mutating the SRE box abolished SREBP-1a binding and transactivation. The in vivo binding of SREBP-1a to the SRE box in the S. aurata PFKFB1 promoter was confirmed by chromatin immunoprecipitation assays. There is a great deal of evidence for a postprandial rise of PFKB1 mRNA levels in fish and rats. Consistently, starved-to-fed transition and treatment with glucose or insulin increased SREBP-1 immunodetectable levels, SREBP-1 association to PFKFB1 promoter, and PFKFB1 mRNA levels in the piscine liver. Our findings demonstrate involvement of SREBP-1a in the transcriptional activation of PFKFB1, and we conclude that SREBP-1a may exert a key role mediating postprandial activation of PFKFB1 transcription.

scholarly journals Role of upstream stimulatory factor 2 in glutamate dehydrogenase gene transcription

2018 ◽  
Vol 60 (3) ◽  
pp. 247-259 ◽  
Author(s):  
Carlos Gaspar ◽  
Jonás I Silva-Marrero ◽  
María C Salgado ◽  
Isabel V Baanante ◽  
Isidoro Metón
Keyword(s):  
Transcriptional Regulation ◽  
Tissue Distribution ◽  
Glutamate Dehydrogenase ◽  
Sea Bream ◽  
Mrna Levels ◽  
Nutritional Regulation ◽  
Upstream Stimulatory Factor ◽  
Hepatic Expression ◽  
Stimulatory Factor

Glutamate dehydrogenase (Gdh) plays a central role in ammonia detoxification by catalysing reversible oxidative deamination of l-glutamate into α-ketoglutarate using NAD+ or NADP+ as cofactor. To gain insight into transcriptional regulation of glud, the gene that codes for Gdh, we isolated and characterised the 5′ flanking region of glud from gilthead sea bream (Sparus aurata). In addition, tissue distribution, the effect of starvation as well as short- and long-term refeeding on Gdh mRNA levels in the liver of S. aurata were also addressed. 5′-Deletion analysis of glud promoter in transiently transfected HepG2 cells, electrophoretic mobility shift assays, chromatin immunoprecipitation (ChIP) and site-directed mutagenesis allowed us to identify upstream stimulatory factor 2 (Usf2) as a novel factor involved in the transcriptional regulation of glud. Analysis of tissue distribution of Gdh and Usf2 mRNA levels by reverse transcriptase-coupled quantitative real-time PCR (RT-qPCR) showed that Gdh is mainly expressed in the liver of S. aurata, while Usf2 displayed ubiquitous distribution. RT-qPCR and ChIP assays revealed that long-term starvation down-regulated the hepatic expression of Gdh and Usf2 to similar levels and reduced Usf2 binding to glud promoter, while refeeding resulted in a slow but gradual restoration of both Gdh and Usf2 mRNA abundance. Herein, we demonstrate that Usf2 transactivates S. aurata glud by binding to an E-box located in the proximal region of glud promoter. In addition, our findings provide evidence for a new regulatory mechanism involving Usf2 as a key factor in the nutritional regulation of glud transcription in the fish liver.

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