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

Abstract

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 (r 2 = 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. Diabetes 50:462-469, 2001

Methodology for studying postprandial lipid metabolism

“…As compared with a control test meal or another test meal, the studied component will be incorporated in the experimental test meal. This will make possible to evaluate the effect of the studied component on the amplitude and/or kinetics of the postprandial lipid response in subjects with normal metabolic homeostasis (Cara et al, 1992;Zampelas et al, 1994a, b;Murphy et al, 1995;Dubois et al, 1998;Roche et al, 1998a, b;Fielding et al, 2000;Harbis et al, 2001Harbis et al, , 2004van Wijk et al, 2001;Sauvant et al, 2003;Jackson et al, 2005).…”

“…The concept behind this type of approach is that a large fat load will overwhelm the normal capacity of lipoprotein handling postprandially and thus, will reveal those subjects with reduced capacity (linked to disturbed metabolism and/or diet), whereas a smaller meal may be insufficient to challenge the metabolic capacity to its limit. Cohen et al (1988) 40-120 Weintraub et al (1988) 50 g/m 2 body surface area Cohn et al (1988aCohn et al ( , 1993 1 g/kg body weight Schneeman (1990) 43 Cara et al (1992) 70 Karpe et al (1993) 50 g/m 2 body surface area Dubois et al (1994a, b) 31/42, 45 Zampelas et al (1994) 40 Frayn et al (1994) 80 Murphy et al (1995) 20-80 Fielding et al (1996) 61 Lopez-Miranda et al (1997) 1 g/kg body weight Lovegrove et al (1997) 82 Roche and Gibney, 1997;Roche et al, 1998a, b 40 Dubois et al (1998 15-50 Couillard et al (1998) 60/m 2 Shishebor et al (1999) 0.5 g/kg body weight Guerci et al (2001) 80 Harbis et al (2001) 40 Dallongeville et al (2002) 70 Harbis et al (2004) 28-29…”

“…Data obtained after addition of glucose (50 and 100 g) to fatty test meals have not been proved consistent in healthy subjects (Cohen and Berger, 1990), whereas addtion of sucrose (Grant et al, 1994) or fructose (Jeppesen et al, 1994) increases postprandial triglyceridaemia. In healthy subjects, starchy foods (white bread, pasta, beans) do not induce noticeable alterations in the overall postprandial triglyceride response but can alter apoB48-containing chylomicrons (Harbis et al, 2001). In subjects with insulin resistance, ingestion of mixed meals with different glycaemic index can modulate the postprandial accumulation of apoB100 and apoB48 containing triacylglycerol-rich lipoproteins (Harbis et al, 2004).…”

“…As mentioned above, postprandial changes in triglyceridaemia are essentially because of TRLs, that is, both intestinally derived chylomicrons and hepatically derived VLDL (Cohn et al, 1993;Schneeman et al, 1993;Karpe et al, 1993Karpe et al, , 1995Roche et al, 1998a;Mekki et al, 1999;Harbis et al, 2001Harbis et al, , 2004. The two main components of these TRL species are triglycerides and apoB.…”

Cholesterol absorption status and fasting plasma cholesterol are modulated by the microsomal triacylglycerol transfer protein −493 G/T polymorphism and the usual diet in women

“…The triglyceride-rich lipoprotein (TRL) fraction (s f = 20-400) was isolated by ultracentrifugation, as previously described [10]. Biochemical analyses were performed with commercial kits on fasting plasma samples as reported in details [43].…”