Dietary Sources of Lysophospholipids
Status: | Recruiting |
---|---|
Conditions: | High Cholesterol, Obesity Weight Loss, Peripheral Vascular Disease |
Therapuetic Areas: | Cardiology / Vascular Diseases, Endocrinology |
Healthy: | No |
Age Range: | 18 - 60 |
Updated: | 9/2/2018 |
Start Date: | July 14, 2015 |
End Date: | December 2020 |
Contact: | Fredrick O Onono, PhD |
Email: | fred.onono@uky.edu |
Phone: | 859-323-3243 |
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.
lysophosphatidylcholine (LPC) acutely alters plasma lysophosphatidic acid (LPA) levels and
autotaxin activity in normal weight and obese subjects.
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.
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.
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.
We found this trial at
1
site
Lexington, Kentucky 40536
Principal Investigator: Susan Smyth, MD
Phone: 859-323-2274
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