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INSERM U-508, Institut Pasteur de Lille, 59019 Lille, France;
Département dAthérosclérose, Institut Pasteur de Lille, 59019 Lille, France;
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Unité INSERM U-476, 18, avenue Mozart, 13009 Marseille Cedex;
INSERM U-545, Institut Pasteur de Lille, 59019 Lille, France;

Service de Nutrition, CHRU de Lille, 59000 Lille, France
2To whom correspondence should be addressed. E-mail: jean.dallongeville{at}pasteur-lille.fr.
The goal of the present study was to compare the plasma lipid responses of massively obese and lean women to a fat load and a carbohydrate load. For this purpose, 11 lean [body mass index (BMI), 21.6 ± 2 kg/m2] and 8 obese (BMI, 50.8 ± 7 kg/m2) normolipidemic women were given, in random order, either a dietary carbohydrate load (3.43 MJ, 166 g carbohydrates, 38 g proteins) or a dietary fat load (3.35 MJ, 70 g fat, 36 g proteins). Blood samples were collected hourly for 9 h after the test meal for measurements of triglyceride-rich lipoprotein (TRL)-lipid, apolipoprotein (apo)B-48 and apoB-100. Triglycerides (P < 0.0001), TRL triglycerides (P < 0.0001), TRL cholesterol (P < 0.04) and apoB-48 (P < 0.0001) peaked 3 h after the fat meal and returned progressively to baseline values in both obese women and lean controls. These lipid and apolipoprotein changes did not differ between the two groups. In contrast, after the carbohydrate load, the plasma triglyceride (P < 0.0001) and TRL triglyceride (P < 0.0001) increments were significantly greater in obese women than in lean controls. This carbohydrate-induced TRL triglyceride increment was half of that following the isocaloric fat load. The carbohydrate load did not affect apoB-100 and apoB-48 levels. These findings suggest that postprandial triglyceride metabolism is impaired after a carbohydrate load in normolipidemic massively obese women.
KEY WORDS: triglycerides lipoprotein apolipoprotein obesity carbohydrate lipid humans
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