The Role of Arachidonic Acid Metabolites, From Patients With Metabolic Syndrome

NCT ID: NCT02498119

Last Updated: 2016-06-21

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

UNKNOWN

Total Enrollment

12 participants

Study Classification

OBSERVATIONAL

Study Start Date

2014-11-30

Study Completion Date

2016-09-30

Brief Summary

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The purpose of this study is to determine whether an increase in lipid bodies in leukocytes will lead to an increase in eicosanoid production. The 2nd purpose is to determine if there is a significant correlation between lipid body formation and enhanced generation of both Lipoxygenase (LO) and COX derived eicosanoids. The 3rd purpose is, if lipid bodies are involved in arachidonic acid (AA) metabolism, then AA present in these lipid rich structure must be released by phospholipases and the free Arachidonic Acid (AA) must have access to the eicosanoid forming enzyme. The fourth objective is to determine the compartmentalisation of cPLA2 and MAP kinases including ERK1, ERK2, p85 and p38 are involved in AA liberation within lipid bodies.

Detailed Description

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Metabolic syndrome is a cluster of biochemical and physiological abnormalities associated with the development of cardiovascular disease and type 2 diabetes mellitus. The current study focused on type 2 Diabetes Mellitus(T2DM). T2DM is a chronic disease in which people have problems regulating their blood sugar. This disorder consists of an array of dysfunctions characterized by hyperglycemia and resulting from the combination of resistance of insulin action, inadequate insulin secretion and excessive or inappropriate glucagon secretion. Insulin resistance results from a complex interplay between nutrient overload, systemic fatty acid excess, inflammation of the adipose tissue, endoplasmic reticulum and oxidative stress.

At the molecular lever, inflammatory cytokines, fatty acid derivatives such as ceramides, diacylglycerols and reactive oxygen species (ROS), activate several serine/threonine kinases, that have emerged as important negative regulators of insulin signaling. Because of their ability to directly oxidize DNA, protein and lipid damage, ROS are believed to play a key role in the metabolic syndrome and the possible development of T2DM. It is possible that ROS and oxidative stress, induced by elevations in glucose and possibly free fatty acid levels play a key role in causing insulin resistance, and beta cell dysfunction by their ability to activate stress sensitive signaling pathways.

Lipids as signaling intermediates encompass a vast range of molecules with distinct function. The characteristics includes, lipid bodies(LB) are sites for the production of inflammatory mediators and LB within inflammatory cells contain arachidonyl lipids which serve as precursors for eicosanoids. In addition, formation of LB within inflammatory macrophages was positively correlated with augmented increase in prostaglandin E2 (PGE2) in changes. LB also could function as a draining compartment to rapidly uptake and re-acetylate free arachidonic acid with the potentially detrimental outcomes for the host cell.

Macrophage from cells with lipid bodies involves complex and multi step mechanisms that depend on different signaling pathways regulating lipid influx, metabolism storage and mobilization. In view of these clues the investigators have reason to believe that organic anion transporters might be resident or upon stimulation trans located to lipid bodies in order to export the newly synthesized lipid mediators into the cytoplasmic space. Once outside the lipid bodies the eicosanoids can exert intracrine functions or be exported to plasma membrane resident transporters to the extracellular space. Free fatty acids have adverse effects on the mitochondrial function including uncoupling of oxidative phosphorylation and the generation of ROS. Beta cell lipotoxicity has an amplifying effect only if mediated by concurrent hyperglycemia. The association of obesity, fatty acids and oxidative stress with insulin action clearly merits further attention with particular focus on the molecular mechanism.

Conditions

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Type 2 Diabetes Mellitus

Study Design

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Study Time Perspective

PROSPECTIVE

Study Groups

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Normal

Patient sample within the normal range of blood results.

No interventions assigned to this group

Abnormal

Patient sample from freshly diagnosed Type 2 Diabetes Mellitus.

No interventions assigned to this group

Eligibility Criteria

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Inclusion Criteria

* age ≥ 18 to ≤ 60
* Patient diagnosed with Type 2 Diabetes Mellitus within 1 year

Exclusion Criteria

* Patients \< 18 years
* Patients with uncontrolled diabetes, heart failure and sepsis
Minimum Eligible Age

18 Years

Maximum Eligible Age

60 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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University of Malaya

OTHER

Sponsor Role lead

Responsible Party

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Gracie Ong @ Gracie Ong Siok Yan

Senior Consultant

Responsibility Role PRINCIPAL_INVESTIGATOR

Principal Investigators

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Gracie Ong Siok Yan

Role: PRINCIPAL_INVESTIGATOR

Senior Consultant

Locations

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University Malaya Medical Center (UMMC)

Petaling Jaya, Kuala Lumpur, Malaysia

Site Status RECRUITING

Countries

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Malaysia

Central Contacts

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Komathi Perumal

Role: CONTACT

6010-2114913

Facility Contacts

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Gracie Ong Siok Yan

Role: primary

019-3105617

Komathi Perumal

Role: backup

010-2114913

References

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Melo RC, D'Avila H, Wan HC, Bozza PT, Dvorak AM, Weller PF. Lipid bodies in inflammatory cells: structure, function, and current imaging techniques. J Histochem Cytochem. 2011 May;59(5):540-56. doi: 10.1369/0022155411404073. Epub 2011 Mar 23.

Reference Type BACKGROUND
PMID: 21430261 (View on PubMed)

Melo RC, Paganoti GF, Dvorak AM, Weller PF. The internal architecture of leukocyte lipid body organelles captured by three-dimensional electron microscopy tomography. PLoS One. 2013;8(3):e59578. doi: 10.1371/journal.pone.0059578. Epub 2013 Mar 26.

Reference Type BACKGROUND
PMID: 23555714 (View on PubMed)

Tauchi-Sato K, Ozeki S, Houjou T, Taguchi R, Fujimoto T. The surface of lipid droplets is a phospholipid monolayer with a unique Fatty Acid composition. J Biol Chem. 2002 Nov 15;277(46):44507-12. doi: 10.1074/jbc.M207712200. Epub 2002 Sep 6.

Reference Type BACKGROUND
PMID: 12221100 (View on PubMed)

Dichlberger A, Schlager S, Lappalainen J, Kakela R, Hattula K, Butcher SJ, Schneider WJ, Kovanen PT. Lipid body formation during maturation of human mast cells. J Lipid Res. 2011 Dec;52(12):2198-2208. doi: 10.1194/jlr.M019737. Epub 2011 Oct 4.

Reference Type BACKGROUND
PMID: 21971714 (View on PubMed)

Krahmer N, Farese RV Jr, Walther TC. Balancing the fat: lipid droplets and human disease. EMBO Mol Med. 2013 Jul;5(7):973-83. doi: 10.1002/emmm.201100671. Epub 2013 Jun 6.

Reference Type BACKGROUND
PMID: 23740690 (View on PubMed)

Hapala I, Marza E, Ferreira T. Is fat so bad? Modulation of endoplasmic reticulum stress by lipid droplet formation. Biol Cell. 2011 Jun;103(6):271-85. doi: 10.1042/BC20100144.

Reference Type BACKGROUND
PMID: 21729000 (View on PubMed)

Beller M, Thiel K, Thul PJ, Jackle H. Lipid droplets: a dynamic organelle moves into focus. FEBS Lett. 2010 Jun 3;584(11):2176-82. doi: 10.1016/j.febslet.2010.03.022. Epub 2010 Mar 18.

Reference Type BACKGROUND
PMID: 20303960 (View on PubMed)

Brasaemle DL. Thematic review series: adipocyte biology. The perilipin family of structural lipid droplet proteins: stabilization of lipid droplets and control of lipolysis. J Lipid Res. 2007 Dec;48(12):2547-59. doi: 10.1194/jlr.R700014-JLR200. Epub 2007 Sep 18.

Reference Type BACKGROUND
PMID: 17878492 (View on PubMed)

Goodman JM. The gregarious lipid droplet. J Biol Chem. 2008 Oct 17;283(42):28005-9. doi: 10.1074/jbc.R800042200. Epub 2008 Jul 8. No abstract available.

Reference Type BACKGROUND
PMID: 18611863 (View on PubMed)

Blaner WS, O'Byrne SM, Wongsiriroj N, Kluwe J, D'Ambrosio DM, Jiang H, Schwabe RF, Hillman EM, Piantedosi R, Libien J. Hepatic stellate cell lipid droplets: a specialized lipid droplet for retinoid storage. Biochim Biophys Acta. 2009 Jun;1791(6):467-73. doi: 10.1016/j.bbalip.2008.11.001. Epub 2008 Nov 24.

Reference Type BACKGROUND
PMID: 19071229 (View on PubMed)

Dvorak AM, Dvorak HF, Peters SP, Shulman ES, MacGlashan DW Jr, Pyne K, Harvey VS, Galli SJ, Lichtenstein LM. Lipid bodies: cytoplasmic organelles important to arachidonate metabolism in macrophages and mast cells. J Immunol. 1983 Dec;131(6):2965-76.

Reference Type BACKGROUND
PMID: 6315820 (View on PubMed)

Dvorak AM, Hammel I, Schulman ES, Peters SP, MacGlashan DW Jr, Schleimer RP, Newball HH, Pyne K, Dvorak HF, Lichtenstein LM, et al. Differences in the behavior of cytoplasmic granules and lipid bodies during human lung mast cell degranulation. J Cell Biol. 1984 Nov;99(5):1678-87. doi: 10.1083/jcb.99.5.1678.

Reference Type BACKGROUND
PMID: 6436254 (View on PubMed)

Triggiani M, Oriente A, Marone G. Differential roles for triglyceride and phospholipid pools of arachidonic acid in human lung macrophages. J Immunol. 1994 Feb 1;152(3):1394-403.

Reference Type BACKGROUND
PMID: 8301140 (View on PubMed)

Yu W, Bozza PT, Tzizik DM, Gray JP, Cassara J, Dvorak AM, Weller PF. Co-compartmentalization of MAP kinases and cytosolic phospholipase A2 at cytoplasmic arachidonate-rich lipid bodies. Am J Pathol. 1998 Mar;152(3):759-69.

Reference Type BACKGROUND
PMID: 9502418 (View on PubMed)

Triggiani M, Oriente A, Seeds MC, Bass DA, Marone G, Chilton FH. Migration of human inflammatory cells into the lung results in the remodeling of arachidonic acid into a triglyceride pool. J Exp Med. 1995 Nov 1;182(5):1181-90. doi: 10.1084/jem.182.5.1181.

Reference Type BACKGROUND
PMID: 7595189 (View on PubMed)

Silva AR, Pacheco P, Vieira-de-Abreu A, Maya-Monteiro CM, D'Alegria B, Magalhaes KG, de Assis EF, Bandeira-Melo C, Castro-Faria-Neto HC, Bozza PT. Lipid bodies in oxidized LDL-induced foam cells are leukotriene-synthesizing organelles: a MCP-1/CCL2 regulated phenomenon. Biochim Biophys Acta. 2009 Nov;1791(11):1066-75. doi: 10.1016/j.bbalip.2009.06.004. Epub 2009 Jun 30.

Reference Type BACKGROUND
PMID: 19573621 (View on PubMed)

Bozza PT, Bakker-Abreu I, Navarro-Xavier RA, Bandeira-Melo C. Lipid body function in eicosanoid synthesis: an update. Prostaglandins Leukot Essent Fatty Acids. 2011 Nov;85(5):205-13. doi: 10.1016/j.plefa.2011.04.020. Epub 2011 May 12.

Reference Type BACKGROUND
PMID: 21565480 (View on PubMed)

Related Links

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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0059578

The internal architecture of leukocyte lipid body organelles captured by three-dimensional electron microscopy tomography

http://www.ncbi.nlm.nih.gov/pubmed/23740690

Balancing the fat: lipid droplets and human disease

http://www.ncbi.nlm.nih.gov/pubmed/21729000

Is fat so bad? Modulation of endoplasmic reticulum stress by lipid droplet formation

http://www.ncbi.nlm.nih.gov/pubmed/20303960

a dynamic organelle moves into focus

http://www.ncbi.nlm.nih.gov/pubmed/17878492

The perilipin family of structural lipid droplet proteins: stabilization of lipid droplets and control of lipolysis

http://www.jbc.org/content/283/42/28005

The gregarious lipid droplet

http://www.ncbi.nlm.nih.gov/pubmed/19071229

Hepatic stellate cell lipid droplets: a specialized lipid droplet for retinoid storage

http://www.ncbi.nlm.nih.gov/pubmed/6315820

Lipid bodies: cytoplasmic organelles important to arachidonate metabolism in macrophages and mast cells

http://www.ncbi.nlm.nih.gov/pubmed/6436254

Differences in the behavior of cytoplasmic granules and lipid bodies during human lung mast cell degranulation

http://www.ncbi.nlm.nih.gov/pubmed/8301140

Differential roles for triglyceride and phospholipid pools of arachidonic acid in human lung macrophages

http://www.ncbi.nlm.nih.gov/pubmed/9502418

Co-compartmentalization of MAP kinases and cytosolic phospholipase A2 at cytoplasmic arachidonate-rich lipid bodies

http://www.ncbi.nlm.nih.gov/pubmed/7595189

Migration of human inflammatory cells into the lung results in the remodeling of arachidonic acid into a triglyceride pool

http://www.ncbi.nlm.nih.gov/pubmed/19573621

Lipid bodies in oxidized LDL-induced foam cells are leukotriene-synthesizing organelles: a monocyte chemotactic protein 1/ chemokine ligand 2 (MCP-1/CCL2) regulated phenomenon

http://www.ncbi.nlm.nih.gov/pubmed/21565480

Lipid body function in eicosanoids synthesis : An update

Other Identifiers

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RG291-14AFR

Identifier Type: -

Identifier Source: org_study_id

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