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Evidence for impaired lipolysis in abdominally obese men: postprandial study of apolipoprotein B-48– and B-100–containing lipoproteins^1,2,3

¹ From the Lipid Research Center, Laval University Medical Research Center, CHUL Pavilion (CC, JB, and J-PD), the Department of Food Science and Nutrition (CC, NB, NA, and J-PD), and the Division of Kinesiology, Department of Preventive and Social Medicine (AT), Laval University, Québec; the Québec Heart Institute (AP, NA, and J-PD); and the School of Human Kinetics, Faculty of Health Sciences, University of Ottawa (DP).

Background: Abdominal obesity has been associated with postprandial hypertriglyceridemia. The contribution of intestinally and hepatically derived lipoproteins to this exaggerated postprandial lipemic response is not known.

Objective: We examined the associations between body fatness, fat distribution, and postprandial apolipoprotein (apo) B-48 and apo B-100 concentrations measured in triacylglycerol-rich lipoproteins (TRLs).

Design: Dietary fat tolerance was investigated in 50 men aged 28–67 y. The subjects were given a test meal containing 60 g fat/m² body surface area and providing 64% of energy from fat, 18% from carbohydrates, and 18% from protein. The meal provided 7524–9196 kJ, depending on body surface area. Blood samples were collected every 2 h over an 8-h period.

Results: The increase in plasma triacylglycerol after the meal resulted from increases in both apo B-48– and apo B-100–containing lipoproteins. The apo B-100 concentration was the strongest contributor (R² = 69.6%, P = 0.0001) to postprandial triacylglycerol in total TRLs; the postprandial increase in triacylglycerol was best predicted by the apo B-48 concentration (R² = 32.7%, P = 0.0001). Visceral abdominal fat was significantly associated with high postprandial TRL apo B-48 and apo B-100 concentrations (r = 0.30–0.44, P < 0.05). After the meal, the apo B-100 concentration in small TRLs decreased in 12 subjects. These men showed features of the insulin resistance–dyslipidemic syndrome, including more visceral fat (P = 0.07) and an altered fasting metabolic profile.

Conclusion: A lower lipolytic capacity may contribute to the exaggerated and prolonged postprandial lipemia among abdominally obese men.

Key Words: Abdominal obesity • visceral adipose tissue • postprandial lipemia • apolipoprotein B-48 • apolipoprotein B-100 • men • hypertriglyceridemia • triacylglycerol-rich lipoproteins

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