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Anticipated Scientific Contributions of the Lipid Metabolite Autacoids in the Era of Metabolomics | OMICS International
ISSN: 2161-0479
Journal of Autacoids and Hormones

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Anticipated Scientific Contributions of the Lipid Metabolite Autacoids in the Era of Metabolomics

Yun Michael Shim*
University of Virginia, Department of Medicine, Division of Pulmonary & Critical Care, PO BOX 800546, Charlottesville, Va 22908-0546, USA
Corresponding Author : Yun Michael Shim
Department of Medicine
M. D. University of Virginia
Division of Pulmonary & Critical Care
PO BOX 800546, Charlottesville
Va 22908-0546, USA
Tel: 434-924-5219
E-mail: [email protected]
Received May 15, 2012; Accepted May 15, 2012; Published May 17, 2012
Citation: Shim YM (2012) Anticipated Scientific Contributions of the Lipid Metabolite Autacoids in the Era of Metabolomics. J Autacoids 1:e117. doi: 10.4172/2161-0479.1000e117
Copyright: © 2012 Shim YM. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Pathogenesis of human disease is incredibly variable in its penetrance and phenotypic expression based on genetic predisposition. Since the initial completion of the human genome project in 2001 [1], substantial efforts have been dedicated to decipher the connection between the genome and human diseases by numerous experimental approaches. These attempts have led to novel strategies to analyze the variants of genomics, transcriptomes and proteomes. As these strategies became mature, a previously unappreciated biological space, consisting of metabolites, is rapidly becoming the forefront of the latest research interests to complement these older strategies. Metabolites participate in extensive lists of cellular function, and the production of metabolites in cells is usually the final outcome of the genomic, transcriptional and translational variants. Thus, the analyses of metabolites can be envisioned as the most integrated effort to assess the biologic mechanisms of action involving the pathogenesis of human diseases. Recently substantial advances in the technologies have enabled simultaneous identification, quantification and characterization of a large number of metabolites including intra- and extra-cellular signaling molecules, amino acid and carbohydrate metabolism products and lipid metabolites. These efforts collectively are now referred as “metabolomics”.
In the interest of the Journal of Autacoids, these latest events are tremendously exciting because a substantial number of metabolites are a part of the mediators classified within the autacoid families. Prime examples of autacoids are lipid metabolites such as leukotrienes, prostaglandins, and lipoxins which are derived from the metabolism of the arachidonic acid. Since the discovery of the leukotrienes by Samuelsson and colleagues [2,3], lipid metabolites have been found to play extremely important and complex roles during the homeostasis of normal human physiology and pathogenesis of human diseases [4]. Even though numerous studies have described pivotal roles which these autacoid mediators play in human biology, there still exists a substantial gap in attempt to precisely connect these autacoids to phenotypes observed in humans. It has been speculated that the bio-production of the lipid metabolism can be adapted by delicate compensatory regulation. Therefore, it has been postulated that modifying one part of these pathways would lead to complex compensatory modulation of other related-lipid metabolites and would result in unexpected biological responses. This was apparent in the recent experience to exploit the prostaglandin-endoperoxide synthase 2 (COX2) as a pharmacological target for novel non-steroidal anti-inflammatory agents. COX2 inhibitors were initially touted as perfect drugs which can provide desired anti-inflammatory effects by blocking the biosynthesis of the pro-inflammatory prostaglandins while mitigating the risk of GI complication due to mucosal damages [5]. Unfortunately the complexity of the pathways involved in this autacoid family was initially overlooked, and it became apparent that the selective inhibitors of the COX2 would also alter other prostaglandin mediators which may be crucial in the process of cardio-protection [6-9]. Subsequently population-based studies demonstrated an unforeseen effect of the increased incidence of myocardial infarction [10,11]. These experiences have demonstrated that the ‘silo-approach” to narrowly investigate one pathway of the lipid metabolites is inadequate. Such approach has potentials to lead biologists to erroneous conclusions in preclinical models. If metabolomics strategies were applied in this case, these complex interactions within the prostaglandin lipid metabolism may have been discovered earlier, and led to better understanding of the physiologies involved in selectively manipulating the COX2 target. We can also speculate that similar reasons may explain the past difficulties to translate a number of successful preclinical findings targeting the lipid metabolites to the bedside [12-24].
As we celebrate the ten-year anniversary of the post-genomic era, lipid metabolites, a subset of the autacoid mediators, are now poised to play a substantial role within the metabolomics strategy. By providing access to a bio-molecular space occupied by these autacoids, phenol typing based on metabolomics offers a unique opportunity to discover novel biomarkers and mechanistic understanding of the pathways operative in human diseases. Therefore, we anticipate that these potential opportunities will lead to the development of novel strategies for predicting disease susceptibility, diagnosis, risk stratification, prognosis and assessing responses to therapies.


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