Type 2 DiabetesNCT04496154
Omega-3 to Reduce Diabetes Risk in Subjects With High Number of Particles That Carry "Bad Cholesterol" in the Blood
A study testing Omega-3 fatty acids (2.7 g/d, EPA:DHA, 2:1) in people with Type 2 Diabetes and Insulin Sensitivity/Resistance, run by May Faraj, PDt, PhD.
Trial summary
In this project, investigators explored the role of the particles that carry "bad cholesterol" in the blood (termed LDL) that are known to promote heart disease, in the promotion of type 2 diabetes (T2D) in humans. Read more about this study
- Who is it for?
- Ages 45 to 74 yearsHealthy volunteers can take part
- Conditions the study is for
- Type 2 Diabetes, Insulin Sensitivity/Resistance, Inflammatory Response
- What is being tested?
- Omega-3 fatty acids (2.7 g/d, EPA:DHA, 2:1)
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 41 participants
- Where
- No sites listed yet
- Study dates
- 5 Sep 2013to 24 Feb 2020
- Phase
- Interventional
- 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 45 to 74 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- Men and post-menopausal women:
- Having a body mass index (BMI) > 20 kg/m2
- Aged between 45 and 74 years
- Having confirmed menopausal status (FSH ≥ 30 U/l)
- Non-smoker
- Sedentary (less than 2 hours of structured physical exercise (ex: sports club) per week)
- Low alcohol consumption: less than 2 alcoholic drinks/day
Who cannot join
- Subjects with elevated risk of cardiovascular disease (≥ 20% of calculated Framingham Risk Score) who require immediate medical intervention by lipid-lowering agents OR who cannot be placed on a 4 weeks wash-out period from their lipid-lowering medication at screening (i.e. upon admission to IRCM clinic).
- Subjects with systolic blood pressure > 160 mmHg or diastolic blood pressure > 100 mmHg
- Prior history of cardiovascular events (like stroke, transient ischemic attack, myocardial infarction, angina, heart failure...)
- Prior history of cancer within the last 3 years
- Thyroid disease - untreated
- Type 1 or 2 diabetes or fasting glucose > 7.0 mmol/L
Show all 27Show fewer
- Claustrophobia
- Anemia - Hb < 120 g/L
- Creatinine > 100 μmol/L
- Hepatic dysfunction - AST/ALT > 3 times normal limit
- Blood coagulation problems (i.e. bleeding predisposition)
- Autoimmune diseases
- Chronic inflammatory diseases
- Concomitant medications
- Hormone replacement therapy (except thyroid hormone at a stable dose)
- Systemic corticosteroids
- Anti-psychotic medications - psycho-active medication
- Anticoagulant treatment (Aspirin, NSAIDs, warfarin, coumadin..)
- Adrenergic agonist
- Anti-hypertensive
- Weight-loss
- Known substance abuse
- Allergy to seafood or fish
- Cancellation of the same scheduled testing visit, twice
- Lack of time to participate in the full length of the study (18 weeks)
- Have exceeded the annual total allowed radiation dose (like X-ray scans and/or tomography in the previous year or in the year to come) according to the physician's judgement.
- All other medical or psychological conditions deemed inappropriate according to the physician
About this study
Official title: The Inflammasome and Dysfunctional Adipose Tissue: Why Should apoB-lipoproteins be Targeted in Humans
In this project, investigators explored the role of the particles that carry "bad cholesterol" in the blood (termed LDL) that are known to promote heart disease, in the promotion of type 2 diabetes (T2D) in humans. In specific, they investigated how these particles may induce the activation of an immune pathway in human fat tissue leading to multiple anomalies that favors T2D. They also explored whether omega-3 fatty acids, which are the type of fat found in fish oils can counterbalance the negative effects of LDL in fat tissue, thus providing a natural way to help reduce the risk for T2D in subjects with elevated blood LDL.
To do so, 41 subjects who were free of disease or medication affecting metabolism were enrolled at the Montreal Clinical Research Institute between 2013 and 2019 and were placed on an intervention with omega-3 fatty acids supplementation for 12 weeks (2.7 g/day, Triple Strength Omega-3 from Webbers Naturals). Investigators examined the effects of LDL and omega-3 on risk factors for T2D before and after the intervention in the whole body and specifically in fat tissue biopsies taken from the hip region. Eighty percent of the subjects who were enrolled into the study completed the intervention.
Read the detailed description
Diabetes-attributed deaths, mostly type 2 diabetes (T2D), total more than 40,000 per year, out of which 80% are secondary to cardiovascular disease and stroke. Research from the investigators' lab and others suggests that elevated atherogenic apoB-lipoproteins, mostly low-density lipoproteins (LDL) may not be a mere consequence of T2D but also a cause. They reported that high numbers of apoB-lipoproteins (apoB) induce subcutaneous white adipose tissue (WAT) dysfunction and predict several risk factors for T2D in humans. However, mechanisms underlying LDL-induced abnormalities and nutritional approaches to target them remain unexplored.
Strong evidence implicates a specific innate immunity system, the NLRP3 inflammasome/ interleukin 1 beta (IL-1β) pathway in WAT dysfunction and associated T2D risk factors in mice and humans (NLRP3 for Nucleotide-binding domain and Leucine-rich repeat Receptor, containing a Pyrin domain 3). Preliminary evidence from the investigator's lab and their collaborator (Dr Maya Saleh, at McGill University) indicated that native apoB-lipoproteins activate the NLRP3 inflammasome leading to IL-1β secretion in murine bone marrow derived macrophages. On the other hand, fish-oil derived omega-3 fatty acids, eicosapentaenoic and docosahexaenoic acids (EPA and DHA), were reported to inhibit the NLRP3 inflammasome/ IL-1β pathway in immune cells.
Thus, the central hypothesis of this trial was that apoB-lipoproteins act as metabolic danger-associated molecular patterns that activate the NLRP3 inflammasome in WAT leading to WAT dysfunction and associated risks for T2D in humans. This can be treated by EPA and DHA supplementation.
The specific hypotheses examined in 2 parts of this trial, at baseline and post-intervention, were:
Part A: At baseline (mechanisms):
Primary hypothesis:
- Compared to subjects with low plasma apoB, subjects with high plasma apoB have higher WAT NLRP3 inflammasome activity indicated by higher WAT IL-1β secretion. Secondary hypotheses:
- WAT IL-1β secretion is associated with risk factors for T2D (WAT dysfunction, systemic inflammation, postprandial hypertriglyceridemia, insulin resistance and hyperinsulinemia).
- Ex vivo, subjects' native LDL prime and/or activate the NLRP3 inflammasome in subjects' own WAT.
Part B: Post-intervention (treatment of the baseline mechanisms):
Primary hypothesis:
- Compared to subjects with low plasma apoB, twelve-week supplementation with EPA and DHA induces a greater reduction in WAT IL-1β secretion in subjects with high plasma apoB eliminating baseline group-differences. Secondary hypotheses:
- Compared to subjects with low plasma apoB, twelve-week supplementation with EPA and DHA induces a greater reduction in risk factors for T2D in subjects with high plasma apoB.
- Twelve-week supplementation with EPA and DHA reduces the baseline associations of WAT IL-1β secretion with risk factors for T2D
- Ex vivo, EPA and DHA inhibit LDL-induced priming and/or activation of subjects' WAT NLRP3 inflammasome.
Forty-one subjects (34% men) were enrolled in the study, of whom 33 subjects completed the 12-week omega-3 intervention (drop out/exclusion rate = 20%). For statistical analysis, subjects were stratified into 2 groups based on baseline median plasma apoB per sex. The 2 groups with high plasma apoB and low plasma apoB were characterized and compared for the primary and secondary outcomes at baseline and following the omega-3 intervention.
- Conditions
- Type 2 Diabetes, Insulin Sensitivity/Resistance, Inflammatory Response, Fatty Acids, Omega-3
- Being tested
- Omega-3 fatty acids (2.7 g/d, EPA:DHA, 2:1)
- Keywords
- HyperapoB, ApoB-lipoproteins, White adipose tissue, NLRP3 inflammasome, Fat metabolism, Insulin sensitivity and secretion, Systemic inflammation, Eicosapentaenoic acid (EPA), Docosahexaenoic acid (DHA)
- Medical subject headings
- Diabetes Mellitus, Type 2, Insulin Resistance
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Omega-3 fatty acids (2.7 g/d, EPA:DHA, 2:1)Dietary supplement
Triple Strength Omega-3 from Webber Naturals
| Study group | Role | What they receive |
|---|---|---|
| Omega-3 fatty acids | Experimental | 3 oral softgels (600 mg EPA and 300 mg DHA / softgel), Triple Strength Omega-3 from Webber Naturals Receives: Dietary Supplement: Omega-3 fatty acids (2.7 g/d, EPA:DHA, 2:1) |
What is being measured
The primary outcome is the main question the study is designed to answer.
Fasting WAT IL-1β secretion
Accumulation of IL-1β in WAT medium ex vivo (by AlphaLISA)
Measured: Baseline
Fasting WAT IL-1β secretion
Accumulation of IL-1β in WAT medium ex vivo (by AlphaLISA)
Measured: At 12-weeks post-intervention
Secondary outcomes (8)
WAT function and inflammation
Protein and gene expression of a panel of markers related to WAT function (e.g. ADIPOQ, PPARG, HMGCR, SREBP1C and 2) and inflammation (e.g. MCP1, ADGRE1, IL1B, NLRP3, IL10) by immunohistochemistry (relative to a total protein) and RT-qPCR (relative to HPRT).
Measured: Baseline
WAT function and inflammation
Protein and gene expression of a panel of markers related to WAT function (e.g. ADIPOQ, PPARG, HMGCR, SREBP1C and 2) and inflammation (e.g. MCP1, ADGRE1, IL1B, NLRP3, IL10) by immunohistochemistry (relative to a total protein) and RT-qPCR (relative to HPRT).
Measured: Change at 12 weeks from baseline
Postprandial fat metabolism
Area under the 6 hour time curve of plasma triglycerides after a high-fat meal (66% fat)
Measured: Baseline
Postprandial fat metabolism
Area under the 6 hour time curve of plasma triglycerides after a high-fat meal (66% fat)
Measured: Change at 12 weeks from baseline
Systemic inflammation
Fasting plasma inflammatory parameters including IL-1Ra
Measured: Baseline
Systemic inflammation
Fasting plasma inflammatory parameters including IL-1Ra
Measured: Change at 12 weeks from baseline
Insulin sensitivity and secretion
Glucose-induced insulin secretion and insulin sensitivity by Botnia clamps
Measured: Baseline
Insulin sensitivity and secretion
Glucose-induced insulin secretion and insulin sensitivity by Botnia clamps
Measured: Change at 12 weeks from baseline
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted3 Aug 2020
- Study start5 Sep 2013
- Primary completion22 Jan 2020
- Study completion24 Feb 2020
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (8)Papers the sponsor has linked to this study.
- Other trials for Type 2 DiabetesStudies of the same condition, open and under way.
- 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
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Prevention
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Enrolment
- 41 participants (actual)
Sponsor and investigators
- Lead sponsor
- May Faraj, PDt, PhD
- Sponsor type
- University, hospital or other
- Collaborators
- Canadian Institutes of Health Research (CIHR)
- Responsible party
- Sponsor-investigator, May Faraj, PDt, PhD, Institut de Recherches Cliniques de Montreal
- Investigators
- May Faraj, PDt, PhD, Principal investigator, Montreal Clinical Research Institute/ University of Montreal
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT04496154
- Sponsor's protocol ID
- 2013-14 and 2014-756
- Other IDs
- NUT273741
- Status last verified
- Feb 2025
- First submitted
- 29 Jul 2020
- Last updated
- 11 Feb 2025
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No: Biological samples (plasma and adipose tissue) can be made available for analysis by other investigators. However data statistical analysis incorporating complete IPD must be conducted by the research team of Dr May Faraj as per subject consent form.
Publications
Lamantia V, Bissonnette S, Wassef H, Cyr Y, Baass A, Dufour R, Rabasa-Lhoret R, Faraj M. ApoB-lipoproteins and dysfunctional white adipose tissue: Relation to risk factors for type 2 diabetes in humans. J Clin Lipidol. 2017 Jan-Feb;11(1):34-45.e2. doi: 10.1016/j.jacl.2016.09.013. Epub 2016 Oct 3.
PubMed 28391908Bissonnette S, Saint-Pierre N, Lamantia V, Cyr Y, Wassef H, Faraj M. Plasma IL-1Ra: linking hyperapoB to risk factors for type 2 diabetes independent of obesity in humans. Nutr Diabetes. 2015 Sep 28;5(9):e180. doi: 10.1038/nutd.2015.30.
PubMed 26417659Lamantia V, Bissonnette S, Provost V, Devaux M, Cyr Y, Daneault C, Rosiers CD, Faraj M. The Association of Polyunsaturated Fatty Acid delta-5-Desaturase Activity with Risk Factors for Type 2 Diabetes Is Dependent on Plasma ApoB-Lipoproteins in Overweight and Obese Adults. J Nutr. 2019 Jan 1;149(1):57-67. doi: 10.1093/jn/nxy238.
PubMed 30535058Skeldon AM, Faraj M, Saleh M. Caspases and inflammasomes in metabolic inflammation. Immunol Cell Biol. 2014 Apr;92(4):304-13. doi: 10.1038/icb.2014.5. Epub 2014 Feb 11.
PubMed 24518981Lamantia V, Sniderman A, Faraj M. Nutritional management of hyperapoB. Nutr Res Rev. 2016 Dec;29(2):202-233. doi: 10.1017/S0954422416000147. Epub 2016 Nov 8.
PubMed 27821191Faraj M. LDL, LDL receptors, and PCSK9 as modulators of the risk for type 2 diabetes: a focus on white adipose tissue. J Biomed Res. 2020 Mar 12;34(4):251-259. doi: 10.7555/JBR.34.20190124.
PubMed 32701068Bissonnette S, Lamantia V, Ouimet B, Cyr Y, Devaux M, Rabasa-Lhoret R, Chretien M, Saleh M, Faraj M. Native low-density lipoproteins are priming signals of the NLRP3 inflammasome/interleukin-1beta pathway in human adipose tissue and macrophages. Sci Rep. 2023 Nov 1;13(1):18848. doi: 10.1038/s41598-023-45870-1.
PubMed 37914804Lamantia V, Bissonnette S, Beaudry M, Cyr Y, Rosiers CD, Baass A, Faraj M. EPA and DHA inhibit LDL-induced upregulation of human adipose tissue NLRP3 inflammasome/IL-1beta pathway and its association with diabetes risk factors. Sci Rep. 2024 Nov 7;14(1):27146. doi: 10.1038/s41598-024-73672-6.
PubMed 39511203
Study at a glance
From the registry record, last updated by the sponsor on 11 Feb 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Inflammasome and Dysfunctional Adipose Tissue: Why Should apoB-lipoproteins be Targeted in Humans
- ClinicalTrials.gov ID
- NCT04496154
- Acronym / sponsor ID
- 2013-14 and 2014-756
- Conditions
- Type 2 Diabetes, Insulin Sensitivity/Resistance, Inflammatory Response, Fatty Acids, Omega-3
- Keywords
- HyperapoB, ApoB-lipoproteins, White adipose tissue, NLRP3 inflammasome, Fat metabolism, Insulin sensitivity and secretion, Systemic inflammation, Eicosapentaenoic acid (EPA)
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 41 participants (actual)
- Lead sponsor
- May Faraj, PDt, PhDUniversity, hospital or other
- Collaborators
- Canadian Institutes of Health Research (CIHR)
- Study start
- 5 Sep 2013 (actual)
- Primary completion
- 22 Jan 2020 (actual)
- Study completion
- 24 Feb 2020 (actual)
- First posted
- 3 Aug 2020 (actual)
- 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.
In this project, investigators explored the role of the particles that carry "bad cholesterol" in the blood (termed LDL) that are known to promote heart disease, in the promotion of type 2 diabetes (T2D) in humans. In specific, they investigated how these particles may induce the activation of an immune pathway in human fat tissue leading to multiple anomalies that favors T2D. They also explored whether omega-3 fatty acids, which are the type of fat found in fish oils can counterbalance the negative effects of LDL in fat tissue, thus providing a natural way to help reduce the risk for T2D in subjects with elevated blood LDL.
To do so, 41 subjects who were free of disease or medication affecting metabolism were enrolled at the Montreal Clinical Research Institute between 2013 and 2019 and were placed on an intervention with omega-3 fatty acids supplementation for 12 weeks (2.7 g/day, Triple Strength Omega-3 from Webbers Naturals). Investigators examined the effects of LDL and omega-3 on risk factors for T2D before and after the intervention in the whole body and specifically in fat tissue biopsies taken from the hip region. Eighty percent of the subjects who were enrolled into the study completed the intervention.
Detailed description
Diabetes-attributed deaths, mostly type 2 diabetes (T2D), total more than 40,000 per year, out of which 80% are secondary to cardiovascular disease and stroke. Research from the investigators' lab and others suggests that elevated atherogenic apoB-lipoproteins, mostly low-density lipoproteins (LDL) may not be a mere consequence of T2D but also a cause. They reported that high numbers of apoB-lipoproteins (apoB) induce subcutaneous white adipose tissue (WAT) dysfunction and predict several risk factors for T2D in humans. However, mechanisms underlying LDL-induced abnormalities and nutritional approaches to target them remain unexplored.
Strong evidence implicates a specific innate immunity system, the NLRP3 inflammasome/ interleukin 1 beta (IL-1β) pathway in WAT dysfunction and associated T2D risk factors in mice and humans (NLRP3 for Nucleotide-binding domain and Leucine-rich repeat Receptor, containing a Pyrin domain 3). Preliminary evidence from the investigator's lab and their collaborator (Dr Maya Saleh, at McGill University) indicated that native apoB-lipoproteins activate the NLRP3 inflammasome leading to IL-1β secretion in murine bone marrow derived macrophages. On the other hand, fish-oil derived omega-3 fatty acids, eicosapentaenoic and docosahexaenoic acids (EPA and DHA), were reported to inhibit the NLRP3 inflammasome/ IL-1β pathway in immune cells.
Thus, the central hypothesis of this trial was that apoB-lipoproteins act as metabolic danger-associated molecular patterns that activate the NLRP3 inflammasome in WAT leading to WAT dysfunction and associated risks for T2D in humans. This can be treated by EPA and DHA supplementation.
The specific hypotheses examined in 2 parts of this trial, at baseline and post-intervention, were:
Part A: At baseline (mechanisms):
Primary hypothesis:
- Compared to subjects with low plasma apoB, subjects with high plasma apoB have higher WAT NLRP3 inflammasome activity indicated by higher WAT IL-1β secretion. Secondary hypotheses:
- WAT IL-1β secretion is associated with risk factors for T2D (WAT dysfunction, systemic inflammation, postprandial hypertriglyceridemia, insulin resistance and hyperinsulinemia).
- Ex vivo, subjects' native LDL prime and/or activate the NLRP3 inflammasome in subjects' own WAT.
Part B: Post-intervention (treatment of the baseline mechanisms):
Primary hypothesis:
- Compared to subjects with low plasma apoB, twelve-week supplementation with EPA and DHA induces a greater reduction in WAT IL-1β secretion in subjects with high plasma apoB eliminating baseline group-differences. Secondary hypotheses:
- Compared to subjects with low plasma apoB, twelve-week supplementation with EPA and DHA induces a greater reduction in risk factors for T2D in subjects with high plasma apoB.
- Twelve-week supplementation with EPA and DHA reduces the baseline associations of WAT IL-1β secretion with risk factors for T2D
- Ex vivo, EPA and DHA inhibit LDL-induced priming and/or activation of subjects' WAT NLRP3 inflammasome.
Forty-one subjects (34% men) were enrolled in the study, of whom 33 subjects completed the 12-week omega-3 intervention (drop out/exclusion rate = 20%). For statistical analysis, subjects were stratified into 2 groups based on baseline median plasma apoB per sex. The 2 groups with high plasma apoB and low plasma apoB were characterized and compared for the primary and secondary outcomes at baseline and following the omega-3 intervention.
Study design
- Primary purpose
- Prevention
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Omega-3 fatty acids | Experimental | Dietary Supplement: Omega-3 fatty acids (2.7 g/d, EPA:DHA, 2:1)3 oral softgels (600 mg EPA and 300 mg DHA / softgel), Triple Strength Omega-3 from Webber Naturals |
Who may qualify
- Ages
- 45 to 74 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (7 listed)
- Having a body mass index (BMI) > 20 kg/m2
- Aged between 45 and 74 years
- Having confirmed menopausal status (FSH ≥ 30 U/l)
- Non-smoker
- Sedentary (less than 2 hours of structured physical exercise (ex: sports club) per week)
Key exclusion criteria (27 listed)
- Subjects with elevated risk of cardiovascular disease (≥ 20% of calculated Framingham Risk Score) who require immediate medical intervention by lipid-lowering agents OR who cannot be placed on a 4 weeks wash-out period from their lipid-lowering medication at screening (i.e. upon admission to IRCM clinic).
- Subjects with systolic blood pressure > 160 mmHg or diastolic blood pressure > 100 mmHg
- Prior history of cardiovascular events (like stroke, transient ischemic attack, myocardial infarction, angina, heart failure...)
- Prior history of cancer within the last 3 years
- Thyroid disease - untreated
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Omega-3 fatty acids (2.7 g/d, EPA:DHA, 2:1)Triple Strength Omega-3 from Webber Naturals | Dietary supplement | Omega-3 fatty acids |
Primary outcome
Fasting WAT IL-1β secretion
Time frame: Baseline
Accumulation of IL-1β in WAT medium ex vivo (by AlphaLISA)
Fasting WAT IL-1β secretion
Time frame: At 12-weeks post-intervention
Accumulation of IL-1β in WAT medium ex vivo (by AlphaLISA)
8 secondary outcomes
WAT function and inflammation
Time frame: Baseline
WAT function and inflammation
Time frame: Change at 12 weeks from baseline
Postprandial fat metabolism
Time frame: Baseline
Postprandial fat metabolism
Time frame: Change at 12 weeks from baseline
Systemic inflammation
Time frame: Baseline
Systemic inflammation
Time frame: Change at 12 weeks from baseline
Insulin sensitivity and secretion
Time frame: Baseline
Insulin sensitivity and secretion
Time frame: Change at 12 weeks from baseline
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 11 Feb 2025.
- Background: PubMed 28391908Lamantia V, Bissonnette S, Wassef H, Cyr Y, Baass A, Dufour R, Rabasa-Lhoret R, Faraj M. ApoB-lipoproteins and dysfunctional white adipose tissue: Relation to risk factors for type 2 diabetes in humans. J Clin Lipidol. 2017 Jan-Feb;11(1):34-45.e2. doi: 10.1016/j.jacl.2016.09.013. Epub 2016 Oct 3.
- Background: PubMed 26417659Bissonnette S, Saint-Pierre N, Lamantia V, Cyr Y, Wassef H, Faraj M. Plasma IL-1Ra: linking hyperapoB to risk factors for type 2 diabetes independent of obesity in humans. Nutr Diabetes. 2015 Sep 28;5(9):e180. doi: 10.1038/nutd.2015.30.
- Background: PubMed 30535058Lamantia V, Bissonnette S, Provost V, Devaux M, Cyr Y, Daneault C, Rosiers CD, Faraj M. The Association of Polyunsaturated Fatty Acid delta-5-Desaturase Activity with Risk Factors for Type 2 Diabetes Is Dependent on Plasma ApoB-Lipoproteins in Overweight and Obese Adults. J Nutr. 2019 Jan 1;149(1):57-67. doi: 10.1093/jn/nxy238.
- Background: PubMed 24518981Skeldon AM, Faraj M, Saleh M. Caspases and inflammasomes in metabolic inflammation. Immunol Cell Biol. 2014 Apr;92(4):304-13. doi: 10.1038/icb.2014.5. Epub 2014 Feb 11.
- Background: PubMed 27821191Lamantia V, Sniderman A, Faraj M. Nutritional management of hyperapoB. Nutr Res Rev. 2016 Dec;29(2):202-233. doi: 10.1017/S0954422416000147. Epub 2016 Nov 8.
- Background: PubMed 32701068Faraj M. LDL, LDL receptors, and PCSK9 as modulators of the risk for type 2 diabetes: a focus on white adipose tissue. J Biomed Res. 2020 Mar 12;34(4):251-259. doi: 10.7555/JBR.34.20190124.
- Results publication: PubMed 37914804Bissonnette S, Lamantia V, Ouimet B, Cyr Y, Devaux M, Rabasa-Lhoret R, Chretien M, Saleh M, Faraj M. Native low-density lipoproteins are priming signals of the NLRP3 inflammasome/interleukin-1beta pathway in human adipose tissue and macrophages. Sci Rep. 2023 Nov 1;13(1):18848. doi: 10.1038/s41598-023-45870-1.
- Results publication: PubMed 39511203Lamantia V, Bissonnette S, Beaudry M, Cyr Y, Rosiers CD, Baass A, Faraj M. EPA and DHA inhibit LDL-induced upregulation of human adipose tissue NLRP3 inflammasome/IL-1beta pathway and its association with diabetes risk factors. Sci Rep. 2024 Nov 7;14(1):27146. doi: 10.1038/s41598-024-73672-6.
- Individual participant dataSharing planned: No. Biological samples (plasma and adipose tissue) can be made available for analysis by other investigators. However data statistical analysis incorporating complete IPD must be conducted by the research team of Dr May Faraj as per subject consent form.
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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.
May Faraj, PDt, PhD principal investigator
Montreal Clinical Research Institute/ University of Montreal
Questions about this trial
What is this clinical trial studying?
A study testing Omega-3 fatty acids (2.7 g/d, EPA:DHA, 2:1) in people with Type 2 Diabetes and Insulin Sensitivity/Resistance, run by May Faraj, PDt, PhD.
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 7 inclusion and 27 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: finished, as of the sponsor's last update on 11 Feb 2025. Status can change between updates, so confirm with the study contact before making plans.
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?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Fasting WAT IL-1β secretion (time frame: Baseline). The study lists 2 primary outcomes in all. 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 NCT04496154, which also lists 8 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 11 Feb 2025; AzTrials last refreshed its copy on 7 Nov 2026.