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Acute Hyperinsulinism Modulates Plasma Apolipoprotein B-48 Triglyceride—Rich Lipoproteins in Healthy Subjects During the Postprandial Period

From INSERM (National Institute of Health and Medical Research) (A.H., C.D., C.J., M.S., D.L.), Marseille; the Service de Nutrition (H.N., C.A.-G., B.V.), Hôpital Sainte-Marguerite, Marseille; UPRES 2193 (H.N., C.A.-G., B.V.), Université de la Méditerranée, Marseille; Bledina sa (C.L.), Villefranche-sur-Saône; Service d'Endocrinologie (B.D.), Centre Hospitalier du Pays d'Aix, Aix-en Provence; Laboratoire Central de Biochimie-Hématologie (H.P.), Hôpital Sainte-Marguerite, Marseille; and Laboratoire de Chimie Analytique (C.D.), Faculté de Pharmacie, Marseille, France.

Address correspondence and reprint requests to Denis Lairon, PhD, Research Director, INSERM U476,18 avenue Mozart, 13009 Marseille, France. E-mail: lairon{at}marseille.inserm.fr .

The role of postprandial insulin in the regulation of postprandial lipid metabolism is still poorly understood. The roles of hyperinsulinemia and insulin resistance in the alteration of postprandial lipid metabolism are not clear either. To improve knowledge in this area, we submitted healthy men to acute hyperinsulinemia in two different ways. In the first study, we compared in 10 men the effects of four isolipidic test meals that induce different degrees of hyperinsulinemia on postprandial lipid metabolism. Three different carbohydrate sources were compared according to their glycemic indexes (GIs; 35, 75, and 100 for white kidney bean, spaghetti, and white bread test meals, respectively); the fourth test meal did not contain any carbohydrates. Postprandial plasma insulin levels were proportional to the GIs (maximal plasma insulin concentrations: 113 ± 16 to 266 ± 36 pmol/l). We found a strong positive correlation during the 6-h postprandial period between apolipoprotein (apo) B-48 plasma concentration and insulin plasma concentration (r² = 0.70; P = 0.0001). In a second study, 5 of the 10 subjects again ingested the carbohydrate-free meal, but during a 3-h hyperinsulinemic- (550 ± 145 pmol/l plasma insulin) euglycemic (5.5 ± 0.8 mmol/l plasma glucose) clamp. A biphasic response was observed with markedly reduced levels of plasma apoB-48 during insulin infusion, followed by a late accumulation of plasma apoB-48 and triglycerides. Overall, the data obtained showed that portal and peripheral hyperinsulinism delays and exacerbates postprandial accumulation of intestinally derived chylomicrons in plasma and thus is involved in the regulation of apoB-48-triglyceride—rich lipoprotein metabolism, in the absence of insulin-resistance syndrome.

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