Transcriptional control mechanisms of genes of lipid and fatty acid metabolism in the Atlantic salmon (Salmo salar L.) established cell line, SHK-1

Minghetti, Matteo; Leaver, Michael J.; Tocher, Douglas R.

doi:10.1016/j.bbalip.2010.12.008

Cited by 142 publications

(137 citation statements)

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“…Lipid metabolism in fish is controlled by some nuclear transcription factors, and PPARs are the most important ones . PPARγ is critical for the regulation of lipogenesis and lipid storage, and PPARα has been implicated in fatty acid catabolism (Ribet et al, 2010;Minghetti et al, 2011). The findings of the present study indicate that insulin injection significantly influences mRNA levels of PPARα and PPARγ, suggesting that they mediate the insulin-induced change of lipid metabolism, in agreement with other studies (Zhuo et al, 2014;Cruz-Garcia et al, 2015;Zheng et al, 2015b).…”

Section: Discussionsupporting

confidence: 82%

Effect and the related signaling pathways of insulin influencing lipid metabolism in yellow catfishPelteobagrus fulvidraco

Zhuo

Luo

Pan

et al. 2015

Journal of Experimental Biology

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The influence of insulin on hepatic metabolism in fish is not well understood. The present study was therefore conducted to investigate the effects of insulin on lipid metabolism, and the related signaling pathways, in the yellow catfish Pelteobagrus fulvidraco. Hepatic lipid and intracellular triglyceride (TG) content, the activity and expression levels of several enzymes and the mRNA expression of transcription factors (PPARα and PPARγ) involved in lipid metabolism were determined. Troglitazone, GW6471, fenofibrate and wortmannin were used to explore the signaling pathways by which insulin influences lipid metabolism. Insulin tended to increase hepatic lipid accumulation, the activity of lipogenic enzymes (6PGD, G6PD, ME, ICDH and FAS) and mRNA levels of FAS, G6PD, 6PGD, CPT IA and PPARγ, but down-regulated PPARα mRNA level. The insulin-induced effect could be stimulated by the specific PPARγ activator troglitazone or reversed by the PI3 kinase/Akt inhibitor wortmannin, demonstrating that signaling pathways of PPARγ and PI3 kinase/Akt were involved in the insulin-induced alteration of lipid metabolism. The specific PPARα pathway activator fenofibrate reduced insulininduced TG accumulation, down-regulated the mRNA levels of FAS, G6PD and 6PGD, and up-regulated mRNA levels of CPT IA, PPARα and PPARγ. The specific PPARα pathway inhibitor GW6471 reduced insulin-induced changes in the expression of all the tested genes, indicating that PPARα mediated the insulin-induced changes of lipid metabolism. The present results contribute new knowledge on the regulatory role of insulin in hepatic metabolism in fish.

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Section: Discussionsupporting

confidence: 82%

Effect and the related signaling pathways of insulin influencing lipid metabolism in yellow catfishPelteobagrus fulvidraco

Zhuo

Luo

Pan

et al. 2015

Journal of Experimental Biology

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“…The critical roles of SREBP-1 and PPAR-α in lipid/fatty acid homeostasis makes the study on fish SREBP-1 and PPAR-α indispensable for the research into lipid and fatty acid nutrition of fish (Chinetti et al, 2000;Horton, 2002;Horton et al, 2002;Ibabe et al, 2002;Nakamura et al, 2004;Minghetti et al, 2011;Cunha et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

“…SREBP-la may be responsible for maintaining basal levels of cholesterol and fatty acid synthesis in vivo, while a number of studies in mammals have demonstrated that SREBP-1c predominantly acts to increase the expression of genes involved in fatty acid synthesis, including fatty acid synthase (FAS), fatty acid desaturase (Fad), and elongase of very long chain fatty acid (Elovl) genes Kumadaki et al, 2008;Qin et al, 2009). In fish, however, so far only one single form of SREBP-1 gene has been characterized (Minghetti et al, 2011), and it is unknown whether it has functions of both SREBP-1a and c genes in mammals. Limited studies on fish have implied that SREBP-1 are important transcriptional regulators of salmon Δ6 Fad (Zheng et al, 2009) and the gene expression of salmon SREBP-1 could be regulated by DHA and EPA (Minghetti et al, 2011).…”

Section: Introductionmentioning

confidence: 98%

“…In fish, however, so far only one single form of SREBP-1 gene has been characterized (Minghetti et al, 2011), and it is unknown whether it has functions of both SREBP-1a and c genes in mammals. Limited studies on fish have implied that SREBP-1 are important transcriptional regulators of salmon Δ6 Fad (Zheng et al, 2009) and the gene expression of salmon SREBP-1 could be regulated by DHA and EPA (Minghetti et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Cloning and characterization of SREBP-1 and PPAR-α in Japanese seabass Lateolabrax japonicus, and their gene expressions in response to different dietary fatty acid profiles

Dong

Mai

et al. 2015

Comparative Biochemistry and Physiology Part B: Biochemistry an

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“…LNA) concentration may also stimulate expression (Cleveland et al, 2012). Either way, dietary PUFA are likely to exert their effects through molecular mechanism(s) involving their role as ligands of key transcription factors such as sterol regulatory element binding proteins (SREBP) (Minghetti et al, 2011;Carmona-Antoñanzas et al, 2014). Irrespective of mechanism, the up-regulation of LC-PUFA biosynthesis is not sufficient to maintain tissue EPA and DHA in fish fed VO-fed at the same level as in fish fed FO (Bell and Tocher, 2009b;Tocher et al, 2011).…”

Section: Lc-pufa Biosynthesismentioning

confidence: 99%

Omega-3 long-chain polyunsaturated fatty acids and aquaculture in perspective

2015

Self Cite

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Abbreviations: ARA, arachidonic acid (20:4n-6); CVD, cardiovascular disease; DHA, docosahexaenoic acid (22:6n-3); DPA, docosapentaenoic acid (22:5n-3); EFA, essential fatty acid; Elovl, fatty acid elongase; EPA, eicosapentaenoic acid (20:5n-3); Fads, fatty acyl desaturase; FM, fishmeal; FO, fish oil; LC-PUFA, long-chain polyunsaturated fatty acids (≥ C20 ≥ 3 double bonds); LOA, linoleic acid (18:2n-6); LNA, linolenic acid (18:3n-3); PUFA, polyunsaturated fatty acid; TAG, triacylglycerol; VO, vegetable oil. ABSTRACTIn the 40 years since the essentiality of polyunsaturated fatty acids (PUFA) in fish was first established by determining quantitative requirements for 18:3n-3 and 18:2n-6 in rainbow trout, essential fatty acid (EFA) research has gone through distinct phases. For 20 years the focus was primarily on determining qualitative and quantitative EFA requirements of fish species. Nutritional and biochemical studies showed major differences between fish species based on whether C 18 PUFA or long-chain (LC)-PUFA were required to satisfy requirements. In contrast, in the last 20 years, research emphasis shifted to determining "optimal" levels of EFA to support growth of fish fed diets with increased lipid content and where growth expectations were much higher. This required greater knowledge of the roles and functions of EFA in metabolism and physiology, and how these impacted on fish health and disease. Requirement studies were more focused on early life stages, in particular larval marine fish, defining not only levels, but also balances between different EFA. Finally, a major driver in the last 10-15 years has been the unavoidable replacement of fish oil and fishmeal in feeds and the impacts that this can have on n-3 LC-PUFA contents of diets and farmed fish, and the human consumer. Thus, dietary n-3 in fish feeds can be defined by three levels.Firstly, the minimum level required to satisfy EFA requirements and thus prevent nutritional pathologies. This level is relatively small and easy to supply even with today's current high demand for fish oil. The second level is that required to sustain maximum growth and optimum health in fish being fed modern high-energy diets. The balance between different PUFA and LC-PUFA is important and defining them is more challenging, and so ideal levels and balances are still not well understood, particularly in relation to fish health. The third level is currently driving much research; how can we supply sufficient n-3 LC-PUFA to maintain the nutritional quality of farmed fish at the same level as 20 years ago, and similar or better than in wild fish? This level far exceeds the biological requirements of the fish itself and to satisfy it we require entirely new sources of n-3 LC-PUFA. We cannot rely on the finite and limited marine resources that we can sustainably harvest or 3 efficiently recycle. We need to produce n-3 LC-PUFA de novo and all possible options should be considered.Keywords: Fish oil; essential fatty acids; nutrition; health; metabolism; sustainability 4 Highl...

show abstract

Transcriptional control mechanisms of genes of lipid and fatty acid metabolism in the Atlantic salmon (Salmo salar L.) established cell line, SHK-1

Cited by 142 publications

References 49 publications

Effect and the related signaling pathways of insulin influencing lipid metabolism in yellow catfishPelteobagrus fulvidraco

Effect and the related signaling pathways of insulin influencing lipid metabolism in yellow catfishPelteobagrus fulvidraco

Cloning and characterization of SREBP-1 and PPAR-α in Japanese seabass Lateolabrax japonicus, and their gene expressions in response to different dietary fatty acid profiles

Omega-3 long-chain polyunsaturated fatty acids and aquaculture in perspective

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