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Intestines and Liver Contribution to Fasting Postprandial Hypertriglyceridemia

Not Applicable
Completed
Conditions
Metabolic Syndrome
Hypertriglyceridemia
Interventions
Other: Postprandial test
Registration Number
NCT02898142
Lead Sponsor
Assistance Publique - Hôpitaux de Paris
Brief Summary

Fasting and postprandial hypertriglyceridemia (HTG) depends on increased production of intestinal triglyceride rich lipoproteins in patients with isolated fasting hypertriglyceridemia.

The objective of this study is to compare the serum apoB48 rate after a standardized load test, among patients with isolated hypertriglyceridemia and patients with metabolic syndrome.

Detailed Description

Two major studies in 2007 showed that the occurrence of myocardial infarction and death was more frequent in subjects with the highest "non-fasting" triglycerides level. This is an important point that supports the hypothesis that the development of atheromatous lesions also depends on "remnant" of triglyceride-rich lipoproteins (TRL) products such as chylomicrons in the intestine. The elevation of triglycerides in postprandial period depends on the intestinal production of TRL that can be excessively increased as has been shown in diabetes. Accordingly, it is necessary to distinguish between hepatic and intestinal production of TRL in hypertriglyceridemic patients particularly during postprandial period. TRL contain a single molecule of apolipoprotein B (apoB), apoB100 when produced by the liver or apoB-48 when they are produced by the gut. It is well known that apo B100 is the lipoprotein of the VLDL which is increased in hypertriglyceridemia. But preliminary works showed that fasting concentrations of apoB48 were correlated with triglycerides in some hypertriglyceridemic patients. These results suggest an intestinal part in fasting triglycerides levels. It therefore appears that the liver and intestine contribute to hypertriglyceridemia, but the intestinal part is not established particularly in isolated hypertriglyceridemia. The detection of abnormalities in the production of LRT would consider intestinal bowel as a target organ for the initiation of specific lipid-lowering therapy.

Recruitment & Eligibility

Status
COMPLETED
Sex
All
Target Recruitment
39
Inclusion Criteria

Not provided

Exclusion Criteria

Not provided

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
HTG with metabolic syndromePostprandial testPostprandial test : The preparation used for this test consists of a semi standardized liquid meal (400 ml energy drink Fresubin® 2 cal / ml, Fresenius Kabi, France), containing 800 kcal, 50% calories from carbohydrates, 15% in as protein, and 35% as lipid. The test meal will be performed in the morning during 6 hours (between 8:00 and 14:00) after 10 hours of fasting.
Isolated HTG without metabolic syndromePostprandial testPostprandial test : The preparation used for this test consists of a semi standardized liquid meal (400 ml energy drink Fresubin® 2 cal / ml, Fresenius Kabi, France), containing 800 kcal, 50% calories from carbohydrates, 15% in as protein, and 35% as lipid. The test meal will be performed in the morning during 6 hours (between 8:00 and 14:00) after 10 hours of fasting.
Primary Outcome Measures
NameTimeMethod
Apo B48 plasma concentrationevery hour for 6 hours (day of sampling after postprandial test)

Area under the Apo B48 (g/L) plasma concentration (g/L) measured every hour for 6 hours versus time curve (AUC).

Secondary Outcome Measures
NameTimeMethod
Apo B48 peak plasma concentrationthe highest level of Apo B48 during the test of 6 hours (day of sampling after postprandial test)

Apo B48 (g/L) peak plasma concentration (Cmax)

Trial Locations

Locations (1)

Pitié Salpetriere Hospital

🇫🇷

Paris, France

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