Acute hyperinsulinism modulates plasma apolipoprotein B-48 triglyceride-rich lipoproteins in healthy subjects during the postprandial period

Citation
A. Harbis et al., Acute hyperinsulinism modulates plasma apolipoprotein B-48 triglyceride-rich lipoproteins in healthy subjects during the postprandial period, DIABETES, 50(2), 2001, pp. 462-469
Citations number
52
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
DIABETES
ISSN journal
00121797 → ACNP
Volume
50
Issue
2
Year of publication
2001
Pages
462 - 469
Database
ISI
SICI code
0012-1797(200102)50:2<462:AHMPAB>2.0.ZU;2-K
Abstract
The role of postprandial insulin in the regulation of postprandial lipid me tabolism is still poorly understood. The roles of hyperinsulinemia. and ins ulin resistance in the alteration of postprandial lipid metabolism are not clear either. To improve knowledge in this area, me submitted healthy men t o acute hyperinsulinemia in two different ways. In the first study, we comp ared in 10 men the effects of four isolipidic test meals that induce differ ent degrees of hyperinsulinemia on postprandial lipid metabolism. Three dif ferent carbohydrate sources mere compared according to their glycemic index es (GIs; 35, 75, and 100 for white kidney bean, spaghetti, and white bread test meals, respectively); the fourth test meal did not contain any carbohy drates. Postprandial plasma insulin levels mere proportional to the GIs (ma ximal plasma insulin concentrations; 113 +/- 16 to 266 +/- 36 pmol/l). We f ound a strong positive correlation during the 6-h postprandial period betwe en apolipoprotein (apo) B-48 plasma concentration and insulin plasma concen tration (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 hyperinsulinemi c- (550 +/- 145 pmol/l plasma insulin) euglycemic (5.5 +/- 0.8 mmol/l plasm a glucose) clamp. A biphasic response was observed with markedly reduced le vels of plasma apoB-48 during insulin infusion, followed by a late accumula tion of plasma apoB-48 and triglycerides. Overall, the data obtained showed that portal and peripheral hyperinsulinism delays and exacerbates postpran dial accumulation of intestinally derived chylomicrons in plasma and thus i s involved in the regulation of apoB-48-triglyceride-rich lipoprotein metab olism, in the absence of insulin-resistance syndrome.