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Purpose

This study aims to test the hypothesis that dietary intake of phosphatidylcholine (PC) and lysophosphatidylcholine (LPC) acutely alters plasma lysophosphatidic acid (LPA) levels and autotaxin activity in normal weight and obese subjects.

Conditions

Eligibility

Eligible Ages
Between 18 Years and 60 Years
Eligible Genders
All
Accepts Healthy Volunteers
Yes

Inclusion Criteria

  • Age 18 to 60 years old - Body Mass Index of 20 and above - Must be able to consume a low fat meal, unlimited fruits and vegetables and not eating after midnight the night before the lipid tolerance test - Report to the clinical research unit fasting (no food since the meal the night before) - Able to consume a liquid meal consisting of a commercial nutritional product supplemented with fat - Able to have an indwelling catheter placed on one arm and have hourly blood draws for 8 hours

Exclusion Criteria

  • Unstable medical condition (recent or unstable cardiovascular disease) - Active cancer - Renal insufficiency Glomerular Filtration Rate <30 - Use of steroids - Chronic inflammatory conditions - Use of anticoagulants, anti-inflammatory, or lipid-lowering medications - Lipodystrophy - GI conditions that result in lipid intolerance - Pregnant women have a tendency to be anemic and therefore will be excluded.

Study Design

Phase
Study Type
Observational
Observational Model
Cohort
Time Perspective
Prospective

Arm Groups

ArmDescriptionAssigned Intervention
Healthy BMI is between 20 and 25
Overweight BMI is between 25 and 30
Obese BMI is between 30 and 40

Recruiting Locations

More Details

NCT ID
NCT02952638
Status
Terminated
Sponsor
Susan Smyth

Detailed Description

Lysophosphatidic acid (LPA) is a simple glycerophospholipid that is found at biologically-relevant levels in plasma and has important effects on isolated or cultured blood, vascular and fat cells. The main enzyme responsible for generation of plasma LPA is the secreted lysophospholipase D, autotaxin (ATX). Adipocytes contribute substantially to plasma ATX levels. The investigators have demonstrated rapid production and metabolism of plasma LPA in animals. More recently, the investigators have observed that plasma LPA levels increase in mice fed a high fat ("Western") diet in comparison to levels found in mice fed normal chow. The investigators have also found that diet-induced obesity increased circulating ATX levels in mice. The investigators hypothesize that diet, and in particular dietary phosphatidylcholine (PC), may regulate the autotaxin substrate lysophosphatidylcholine (LPC), from which LPA is derived. Obesity may amplify the response by increasing plasma ATX levels and/or activity. The current study will test whether dietary PC in normal weight and obese subjects acutely alters LPA levels and autotaxin activity.

Notice

Study information shown on this site is derived from ClinicalTrials.gov (a public registry operated by the National Institutes of Health). The listing of studies provided is not certain to be all studies for which you might be eligible. Furthermore, study eligibility requirements can be difficult to understand and may change over time, so it is wise to speak with your medical care provider and individual research study teams when making decisions related to participation.