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Postprandial Fatty Acid Metabolism in Subjects With Lipoprotein Lipase Deficiency

Study acronym: AGL12
StatusRecruiting
PhaseNot applicable
Started
View on ClinicalTrials.gov ↗

Record History

  1. Primary completion date: Sep 30, 2025 to Dec 30, 2026
    • Study completion date: Dec 30, 2025 to Mar 30, 2027
    v8
  2. Primary completion date: Jul 30, 2024 to Sep 30, 2025
    • Study completion date: Dec 30, 2024 to Dec 30, 2025
    v7
  3. Primary completion date: Dec 30, 2023 to Jul 30, 2024
    • Study completion date: Dec 30, 2023 to Dec 30, 2024
    v6
  4. Primary completion date: Aug 30, 2022 to Dec 30, 2023
    • Study completion date: Dec 30, 2022 to Dec 30, 2023
    v5
  5. Primary completion date: Jul 30, 2022 to Aug 30, 2022v4
Show 2 earlier versionsHide 2 earlier versions
  1. Primary completion date: Mar 2021 to Jul 30, 2022
    • Study completion date: Jun 2021 to Dec 30, 2022
    v3
  2. Secondary endpoints: details revised at 1 of 10 entriesv2
  1. Study First Submitted
  • Stopped: an ongoing trial was terminated, suspended or withdrawn.
  • Notable: the trial’s plan changed such as a big move in its timeline or size, a new primary endpoint, sponsor or phase, or recruiting opened or resumed.
  • Minor: routine progress and housekeeping, such as sites added or enrollment closed.
Lipoprotein lipase (LPL) is an enzyme that plays an important role in removing triglycerides (TG) (molecules that transport dietary fat) from the blood. Patients with LPL deficiency (LPLD) display during their whole life very high plasma TG levels often associated with episodes of postprandial abdominal pain, malaise, blurred vision, dizziness (hyperchylomicronemia syndrome) that may lead to recurrent pancreatitis episodes. Because of their very slow clearance in blood of their chylomicron-TG, these patients need to severely restrict their dietary fat intake to avoid these complications. Fortunately, novel treatments are being developed to circumvent LPL deficiency (LPLD) metabolic effect on chylomicron-TG clearance. However, there is no data on how LPLD affect organ-specific dietary fatty acid metabolism nor how the novel therapeutic agents may change this metabolism. For example, it is currently not understood how subjects with LPLD store their DFA into adipose tissues and whether they are able to use DFA as a fuel to sustain their cardiac metabolism, as healthy individuals do. This study aims to better understand theses two questions.
Trial Details
NCT Number NCT04227678
Lead Sponsor Université de Sherbrooke
Collaborators: Institut de Recherches Cliniques de Montreal
Conditions
(from sponsor)		 Lipoprotein Lipase Deficiency
Related terms Hyperlipoproteinemia Type I
Enrollment 16 participants
Start Date
Primary Completion (estimated)
Study Completion (estimated)
Updated on ClinicalTrials.gov