Type 2 Diabetes MellitusNCT02498119
The Role of Arachidonic Acid Metabolites, From Patients With Metabolic Syndrome
An observational study of Type 2 Diabetes Mellitus, run by University of Malaya at 1 site in Malaysia.
Trial summary
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… Read more about this study
- Who is it for?
- Ages 18 to 60 yearsHealthy volunteers can take part
- Conditions the study is for
- Type 2 Diabetes Mellitus
- How many people
- 12 participants
- Where
- 1 siteMalaysia
- Study dates
- Nov 2014to Sep 2016
- How long will I take part?
- 12 Months
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 60 years
- All sexes
- Healthy volunteers accepted
- Adult
Study population: The study subjects are recruited from Primary Care Clinic of University Malaya Medical Center
Who may be able to join
- age ≥ 18 to ≤ 60
- Patient diagnosed with Type 2 Diabetes Mellitus within 1 year
Who cannot join
- Patients < 18 years
- Patients with uncontrolled diabetes, heart failure and sepsis
Trial locations and contacts
1 site in 1 country.
Malaysia1 site, 1 recruiting
- Recruiting
University Malaya Medical Center (UMMC)
Petaling Jaya, Kuala Lumpur, 50603
Gracie Ong Siok Yan, 019-3105617, gracieong@gmail.com
Komathi Perumal, 010-2114913, komathi_thesis@yahoo.com
About this study
Official title: The Role of Arachidonic Acid Metabolites, in the Lipid Droplets of Macrophages From Patients With Metabolic Syndrome
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.
Read the detailed description
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
- Type 2 Diabetes Mellitus
- Keywords
- Type 2 DM, lipid bodies
- Medical subject headings
- Diabetes Mellitus, Type 2
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Normal | Patient sample within the normal range of blood results. | |
| Abnormal | Patient sample from freshly diagnosed Type 2 Diabetes Mellitus. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Composite measure of patient physical observations to include weight, height and BMI
Measured: six months only (1 time only)
Secondary outcomes (3)
Reduction of pro - inflammatory cytokines
Measured: one year
The effect of eicosanoids in diabetic complication
Measured: One year
The effect of LTB4 and LTC4 of eicosanoids
Measured: One year
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted15 Jul 2015 (estimated)
- Study startNov 2014
- Primary completionJan 2016
- Study completionSep 2016 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (17)Papers the sponsor has linked to this study.
- Other trials for Type 2 Diabetes MellitusStudies of the same condition, open and under way.
- More trials run by University of MalayaThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Time perspective
- Prospective
- Enrolment
- 12 participants (estimated)
- Target duration
- 12 Months
Sponsor and investigators
- Lead sponsor
- University of Malaya
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Gracie Ong @ Gracie Ong Siok Yan, University of Malaya
- Investigators
- Gracie Ong Siok Yan, Principal investigator, Senior Consultant
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02498119
- Sponsor's protocol ID
- RG291-14AFR
- Status last verified
- Jun 2016
- First submitted
- 14 May 2015
- Last updated
- 21 Jun 2016
- Results posted
- No
- Data monitoring committee
- No
Publications
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.
PubMed 21430261Melo 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.
PubMed 23555714Tauchi-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.
PubMed 12221100Dichlberger 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.
PubMed 21971714Krahmer 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.
PubMed 23740690Hapala 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.
PubMed 21729000Beller 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.
PubMed 20303960Brasaemle 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.
PubMed 17878492Goodman 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.
PubMed 18611863Blaner 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.
PubMed 19071229Dvorak 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.
PubMed 6315820Dvorak 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.
PubMed 6436254Triggiani 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.
PubMed 8301140Yu 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.
PubMed 9502418Triggiani 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.
PubMed 7595189
Study at a glance
From the registry record, last updated by the sponsor on 21 Jun 2016. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Role of Arachidonic Acid Metabolites, in the Lipid Droplets of Macrophages From Patients With Metabolic Syndrome
- ClinicalTrials.gov ID
- NCT02498119
- Acronym / sponsor ID
- RG291-14AFR
- Conditions
- Type 2 Diabetes Mellitus
- Keywords
- Type 2 DM, lipid bodies
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 12 participants (estimated)
- Lead sponsor
- University of MalayaUniversity, hospital or other
- Study start
- Nov 2014
- Primary completion
- Jan 2016 (actual)
- Study completion
- Sep 2016 (estimated)
- First posted
- 15 Jul 2015 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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
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.
Study design
- Time perspective
- Prospective
- Target follow-up
- 12 Months
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Normal | – | –Patient sample within the normal range of blood results. |
| Abnormal | – | –Patient sample from freshly diagnosed Type 2 Diabetes Mellitus. |
Who may qualify
- Ages
- 18 to 60 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult
- Study population
- The study subjects are recruited from Primary Care Clinic of University Malaya Medical Center
Key inclusion criteria (2 listed)
- age ≥ 18 to ≤ 60
- Patient diagnosed with Type 2 Diabetes Mellitus within 1 year
Key exclusion criteria (2 listed)
- Patients < 18 years
- Patients with uncontrolled diabetes, heart failure and sepsis
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Composite measure of patient physical observations to include weight, height and BMI
Time frame: six months only (1 time only)
3 secondary outcomes
Reduction of pro - inflammatory cytokines
Time frame: one year
The effect of eicosanoids in diabetic complication
Time frame: One year
The effect of LTB4 and LTC4 of eicosanoids
Time frame: One year
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 21 Jun 2016.
- Background: PubMed 21430261Melo 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.
- Background: PubMed 23555714Melo 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.
- Background: PubMed 12221100Tauchi-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.
- Background: PubMed 21971714Dichlberger 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.
- Background: PubMed 23740690Krahmer 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.
- Background: PubMed 21729000Hapala 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.
- Background: PubMed 20303960Beller 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.
- Background: PubMed 17878492Brasaemle 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.
- Background: PubMed 18611863Goodman 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.
- Background: PubMed 19071229Blaner 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.
- Background: PubMed 6315820Dvorak 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.
- Background: PubMed 6436254Dvorak 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.
- The internal architecture of leukocyte lipid body organelles captured by three-dimensional electron microscopy tomographyLink provided by the sponsor.
- Balancing the fat: lipid droplets and human diseaseLink provided by the sponsor.
- Is fat so bad? Modulation of endoplasmic reticulum stress by lipid droplet formationLink provided by the sponsor.
- a dynamic organelle moves into focusLink provided by the sponsor.
- The perilipin family of structural lipid droplet proteins: stabilization of lipid droplets and control of lipolysisLink provided by the sponsor.
- Hepatic stellate cell lipid droplets: a specialized lipid droplet for retinoid storageLink provided by the sponsor.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Gracie Ong Siok Yan principal investigator
Senior Consultant
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Type 2 Diabetes Mellitus, run by University of Malaya at 1 site in Malaysia.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 2 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 21 Jun 2016. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Malaysia. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Komathi Perumal (6010-2114913, komathi_thesis@yahoo.com), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Composite measure of patient physical observations to include weight, height and BMI (time frame: six months only (1 time only)). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02498119, which also lists 17 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 21 Jun 2016.