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      Apolipoprotein C-III's role in cardiovascular diseases, a short review

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      ScienceOpen Research


      Medicine, ApoC-III, CVD, Hypertriglyceridemia, Mutations

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          In this short review I show the important role played by ApoC-III in the lipid dysregulation present in the majority of cardiovascular diseases. With an emphasis on the mutations present in a minority of individuals that confer protection. With this in mind I state that Apoc-III should be considered a valid target for pharmaceutical intervention and cardiovascular disease control and progression.

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          Common genetic variation in the promoter of the human apo CIII gene abolishes regulation by insulin and may contribute to hypertriglyceridemia.

          Overexpression of plasma apolipoprotein CIII (apo CIII) causes hypertriglyceridemia in transgenic mice. A genetically variant form of the human apo CIII promoter, containing five single base pair changes, has been shown to be associated with severe hypertriglyceridemia in a patient population. In animals and in cultured cells the apo CIII gene is transcriptionally downregulated by insulin. In this study we demonstrate that, unlike the wild-type promoter, the variant promoter was defective in its response to insulin treatment, remaining constitutively active at all concentrations of insulin. The loss of insulin regulation was mapped to polymorphic sites at -482 and -455, which fall within a previously identified insulin response element. Loss of insulin regulation could result in overexpression of the apo CIII gene and contribute to the development of hypertriglyceridemia. The variant apo CIII promoter is common in the human population and may represent a major contributing factor to the development of hypertriglyceridemia.
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            Regulation of hepatic ApoC3 expression by PGC-1β mediates hypolipidemic effect of nicotinic acid.

            Peroxisome proliferator-activated receptor (PPAR) γ coactivator-1β (PGC-1β) is a transcriptional coactivator that induces hypertriglyceridemia in response to dietary fats through activating hepatic lipogenesis and lipoprotein secretion. The expression of PGC-1β is regulated by free fatty acids. Here we show that PGC-1β regulates plasma triglyceride metabolism through stimulating apolipoprotein C3 (APOC3) expression and elevating APOC3 levels in circulation. Remarkably, liver-specific knockdown of APOC3 significantly ameliorates PGC-1β-induced hypertriglyceridemia in mice. Hepatic expression of PGC-1β and APOC3 is reduced in response to acute and chronic treatments with nicotinic acid, a widely prescribed drug for lowering plasma triglycerides. Adenoviral-mediated knockdown of PGC-1β or APOC3 in the liver recapitulates the hypolipidemic effect of nicotinic acid. Proteomic analysis of hepatic PGC-1β transcriptional complex indicates that it stimulates APOC3 expression through coactivating orphan nuclear receptor ERRα and recruiting chromatin-remodeling cofactors. Together, these studies identify PGC-1β as an important regulator of the APOC3 gene cluster and reveal a mechanism through which nicotinic acid achieves its therapeutic effects. Copyright © 2010 Elsevier Inc. All rights reserved.
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              Role of ApoCs in Lipoprotein Metabolism


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                ScienceOpen Research
                18 November 2014
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                [1 ]Universitatea de Medicina si Farmacie “Victor Babeş”
                Author notes
                [* ]Corresponding author's e-mail address: olteanugheorgheemilian@ 123456gmail.com
                © 2014 Olteanu G. Emilian.

                This work has been published open access under Creative Commons Attribution License CC BY 4.0 , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Conditions, terms of use and publishing policy can be found at www.scienceopen.com .

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                Figures: 0, Tables: 0, References: 16, Pages: 3
                Short Review


                ApoC-III, Mutations, Hypertriglyceridemia, CVD


                Comments: In the present study the author summarizes the findings concerning ApoC-III in metabolic imbalance and cardiovascular diseases. This paper focus on mutations present in a minority of individuals and suggests that ApoC-III should be considered as a possible target for pharmacological intervention. Major Comments 1- The abstract does not address the importance of apolipoprotein C in cardiovascular and metabolic disease. I suggest that the abstract be improved and/or complement the abstract with the previously stated information. 2- In the introduction, the sentence “The overall effects of apoC-III modulation in mice models are supported by genetic association studies in various human populations [5]”. Please add more than one reference to justify the use of the pluralized version of the noun, “study”. Alternatively, if it has only one citation, please adjust the plural to the singular. 3- The introduction does not have a clear objective. Please include the main goal(s) of the study to better guide the reader. 4- The author discusses the relationships among the genetic factors related to ApoC diseases and concludes that there ought to be a specific potential therapeutic target, and suggests this target. However, there is no strong argumentation that leads to this conclusion in the text. I believe that would be important to describe at least one potential target and add a figure summarizing this pathway. Minor Comments; In the first paragraph of the topic “function”, the author indicates the concentration of ApoC in human body; however, I suggest that the author checks this value in more current studies. I suggest an overall English review of the manuscript. There are many sentence are difficult to understand.
                2015-01-14 12:52 UTC
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