Control of intestinal lipoprotein secretion by dietary carbohydrates

Abstract

The studies reviewed here have implications for dietary recommendations regarding refined carbohydrate intake and prevention of CVD.

Dietary Impact on Postprandial Lipemia

“…In relation to carbohydrates, according to mechanistic in vivo and in vitro studies by Lewis and colleagues (5), monosaccharides indirectly induce an increase in postprandial plasma lipid levels by stimulating intestinal de novo lipogenesis (in particular fructose) and chylomicron secretion, through the Abbreviations: Apo, apolipoprotein; CHO, carbohydrate; CETP, cholesteryl ester transfer protein; HF-LCHO, high-fat/low-carbohydrate diets; iAUC, incremental area under the curve; LF-HCHO, low-fat/high-carbohydrate diet; MUFA, monounsaturated fatty acid; SFA, saturated fatty acid; PPL, postprandial lipemia; PUFA, polyunsaturated fatty acid; TAG, triglyceride; tAUC, total area under the curve; TEI, total energy intake; TRL, triglyceride-rich lipoproteins; VLDL, very low-density lipoprotein. rapid mobilization of intracellular lipid droplets and preformed chylomicrons.…”

“…In relation to carbohydrates, according to mechanistic in vivo and in vitro studies by Lewis and colleagues ( 5 ), monosaccharides indirectly induce an increase in postprandial plasma lipid levels by stimulating intestinal de novo lipogenesis (in particular fructose) and chylomicron secretion, through the rapid mobilization of intracellular lipid droplets and preformed chylomicrons. Conversely, at the intestinal level, dietary fibers may exert a triglyceride-lowering effect by disrupting the micellization process, altering gut motility, physically impeding fat absorption through the formation of a water barrier between nutrients and intestinal mucosa, and by altering gut microbiota ( 6 ).…”

Effect of Nutrient and Micronutrient Intake on Chylomicron Production and Postprandial Lipemia

“…Besides the effects of dietary carbohydrates on hepatic VLDL metabolism [74,94], their effects on intestinal CM metabolism remain to be clarified, but have been reviewed in a recent paper pointing out the intestine as a contributor to carbohydrate-induced hyperlipidemia [95]. Oral fructose in a mixed meal can stimulate hepatic but also intestinal de novo lipogenesis, thereby increasing TG availability for CM and VLDL synthesis.…”

“…At a cellular level, both luminal and basolateral glucose enhanced CM secretion with a greater effect of luminal glucose and a greater effect of luminal glucose than fructose [95]. In Caco-2/15 cells, basolateral exposure to glucose increased apical cholesterol uptake with increased expression of Niemann-Pick C1-like 1.…”

Dyslipidemia Management in Adults With Diabetes

“…Several pathogenic mechanisms underlie the atherogenic dyslipidemia complex of type 2 diabetes including increased production and secretion of both intestinal and hepatic TG-rich lipoproteins (5). This is mediated in part by incretins such as glucagon like peptide 1 and glucagon like peptide 2 (6) and also bile acids (7).…”