Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease.

Groot, P.H.E.; Stiphout, W A van; Krauss, X. H.; Jansen, Hans; Tol, Arie van; Ramshorst, E. van; Chin-On, S; Hofman, Albert; Cresswell, S R; Havekes, Louis M.

doi:10.1161/01.atv.11.3.653

Cited by 488 publications

(247 citation statements)

References 46 publications

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“…Patients with type III hyperlipoproteinaemia [8], chronic renal failure [40] or NIDDM [41] have elevated levels of remnant lipoproteins as well as accelerated development of atherosclerosis. Finally, elevated postprandial levels of triglycerides or remnant lipoproteins have also been found to be predictors of the presence, severity, progression or familial risk of atherosclerosis [42][43][44][45][46][47][48]. The present results therefore add to the growing evidence that remnant lipoproteins in the postprandial state may be involved directly in promoting atherosclerosis.…”

Section: U Rsupporting

confidence: 68%

Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits

1997

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Coronary heart disease and thus atherosclerosis is the leading cause of death among patients suffering from diabetes mellitus; men and women with diabetes have a three to fivefold higher coronary heart disease mortality or incidence rate compared with non-diabetic subjects [1]. Although a number of factors such as hyperglycaemia, dyslipidaemia, a procoagulant state, hyperinsulinaemia, glycation of proteins, oxidation or glycation of lipoproteins, as well as enhanced smooth muscle cell proliferation and foam cell formation, have all been suggested as possible links between diabetes and atherosclerosis [1], the increased risk of coronary heart disease among diabetic patients still remains largely unexplained.Hyperinsulinaemia could be directly involved in atherogenesis [2], although this possibility is fiercely debated [3][4][5][6]. In patients with insulin-dependent diabetes (IDDM) exogenous hyperinsulinaemia exists due to intermittent injections of large amounts of insulin [1], and in patients with non-insulin dependent diabetes (NIDDM) endogenous hyperinsulinaemia Diabetologia (1997) 40: 512-520 Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits Summary To examine the hypothesis that hyperinsulinaemia promotes atherosclerosis, cholesterol-fed rabbits were injected subcutaneously with 6 IU of human insulin (n = 16) or placebo (n = 20) daily for 24 weeks; injection of insulin resulted in hyperinsulinaemia for up to 16 h after injection. Compared to placebo rabbits, insulin-treated rabbits had higher levels of insulin antibodies in plasma, similar levels of intermediate density, low density and high density lipoprotein cholesterol and similar activities of hepatic and lipoprotein lipase in post-heparin plasma, but lower levels of plasma C-peptide, blood glucose, postprandial plasma triglycerides, plasma cholesterol and very low density lipoprotein cholesterol. On univariate analysis, with and without adjustment for differences in plasma cholesterol levels between the two groups, there were no significant differences in extent or severity of atherosclerosis between insulin and placebo rabbits. Furthermore, after combining the results from all the rabbits to examine plasma insulin levels and the other variables mentioned above as predictors of atherosclerosis severity, plasma insulin level was not a predictor, on univariate or multiple linear regression analysis; the first ranked independent predictors were postprandial intermediate density lipoprotein cholesterol in the arch, and postprandial plasma triglyceride in both the thoracic and abdominal aorta. These results suggest that exogenous hyperinsulinaemia does not promote atherogenesis in cholesterol-fed rabbits, but that postprandial levels of intermediate density lipoprotein cholesterol or plasma triglycerides may be involved in atherogenesis. [Diabetologia (1997)

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Section: U Rsupporting

confidence: 68%

Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits

1997

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“…[Diabetologia (1994) proteins of intestinal origin were higher in patients with NIDDM [2]. In 1979 Zilversmit [3] suggested that triglyceride-rich lipoproteins of intestinal origin, especially the cholesteryl ester-rich chylomicron remnants, could play a very important role in atherogenesis, and since then, several reports have been published supporting this hypothesis [4][5][6][7][8][9][10]. Thus, our observation that postprandial lipaemia was increased in NIDDM raised the possibility that abnormalities in the metabolism of intestinally-derived lipoproteins may contribute to the increased risk of CHD in these patients.…”

Section: Discussionmentioning

confidence: 99%

“…However, the link between a high plasma triglyceride concentration and CHD is far from obvious. For example, patients with NIDDM and/or hypertriglyceridaemia have been shown to have increases in plasminogen activator inhibitor-1 [35,36], smaller, denser LDL particles [37,38], and increased postprandial lipaemia [2,39]; changes which have been proposed as increasing the risk of CHD in non-diabetic subjects [3][4][5][6][7][8][9]. It seems reasonable to speculate that a similar relationship between these changes and CHD would also exist in patients with NIDDM.…”

Section: Discussionmentioning

confidence: 99%

Effect of glipizide treatment on postprandial lipaemia in patients with NIDDM

et al. 1994

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SummaryThe primary goal of the present study was to examine the effects of improved glycaemic control associated with glipizide treatment on postprandial lipaemia in non-insulin-dependent diabetic patients. The metabolism of triglyceride-rich lipoproteins of intestinal origin was assessed by measuring the retinyl palmitate content in plasma and the Svedberg flotation index (Sf) > 400 and Sf 20-400 lipoprotein fractions. Fasting plasma glucose concentrations (14.5 + 0.5 vs 9.0 + 0.5 mmol/1), glycated haemoglobin levels (13.1 + 0.6 vs 9.7 _+ 0.6 %), and daylong plasma glucose concentrations were all significantly lower after glipizide treatment (p < 0.001). The improvement in glycaemic control was associated with increases in insulin-mediated glucose uptake (p < 0.001) and plasma post-heparin lipoprotein and hepatic lipolytic activities Go < 0.02). Both fasting plasma triglyceride (3.09 + 0.51 vs 2.37 + 0.34 mmol/1), and postprandial triglyceride concentrations (p < 0.05-0.001) were lower following glipizide treatment, associated with a significant fall in retinyl palmitate content in all three lipoprotein fractions (p < 0.02-0.001), with the most substantial decrease seen in the Sf 20-400 fraction. These data indicate that glipizide-induced improvement in glycaemic control was associated with changes in the metabolism of triglyceride-rich lipoproteins of intestinal origin that would be anticipated to reduce risk of coronary heart disease in non-insulin-dependent diabetic patients. [Diabetologia (1994) proteins of intestinal origin were higher in patients with NIDDM [2]. In 1979 Zilversmit [3] suggested that triglyceride-rich lipoproteins of intestinal origin, especially the cholesteryl ester-rich chylomicron remnants, could play a very important role in atherogenesis, and since then, several reports have been published supporting this hypothesis [4][5][6][7][8][9][10]. Thus, our observation that postprandial lipaemia was increased in NIDDM raised the possibility that abnormalities in the metabolism of intestinally-derived lipoproteins may contribute to the increased risk of CHD in these patients. Although we could not detect any correlation in our earlier paper between the magnitude of postprandial lipaemia and the level of glycaemic control, the crosssectional nature of the study protocol was not designed to carefully explore such a relationship. Consequently, we initiated the current study to see if improved glycaemic control associated with glipizide

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“…by a huge meta-analysis [5], as well as by intervention [6] and observational long-term [1] studies. In addition, postprandial hyperlipidaemia has been linked to atherosclerosis, even in fasting normocholesterolaemic subjects [7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Overproduction of intestinal lipoprotein containing apolipoprotein B-48 in Psammomys obesus: impact of dietary n-3 fatty acids

et al. 2006

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Aims/hypothesis Emerging evidence underscores the important role of the small intestine in the pathogenesis of dyslipidaemia in insulin resistance and type 2 diabetes. We therefore tested the hypothesis that n-3 fatty acids improve the various events governing intra-enterocyte lipid transport in Psammomys obesus gerbils, a model of nutritionally induced metabolic syndrome. Materials and methods Experiments were carried out on Psammomys obesus gerbils that were assigned to an isocaloric control diet and a diet rich in fish oil for 6 weeks. Results Increased dietary intake of fish oil lowered body weight and improved hyperglycaemia and hyperinsulinaemia. It simultaneously decreased de novo intestinal lipogenesis and lipid esterification of the major lipid classes, e.g. triglycerides, phospholipids and cholesteryl esters, particularly in insulinresistant and diabetic animals. Accordingly, lessened activity of monoacylglycerol and diacylglycerol acyltransferase was recorded. As assessed in cultured jejunal explants incubated with either [ 14 C]-oleic acid or [ 35 S]-methionine, fish oil feeding resulted in diminished triglyceride-rich lipoprotein assembly and apolipoprotein (apo) B-48 biogenesis, respectively. The mechanisms did not involve apo B-48 transcription or alter the gene expression and activity of the critical microsomal triglyceride transfer protein. Rather, the suppressed production of apo B-48 by n-3 fatty acids was associated with intracellular proteasome-mediated posttranslational downregulation in insulin-resistant and diabetic animals. Conclusions/interpretation Our data highlight the beneficial impact of n-3 fatty acids on adverse effects of the metabolic syndrome and emphasise their influence on intestinal lipid transport, an effect which may limit postprandial lipaemia and the risk of atherosclerosis.

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Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease.

Cited by 488 publications

References 46 publications

Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits

Effect of exogenous hyperinsulinaemia on atherogenesis in cholesterol-fed rabbits

Effect of glipizide treatment on postprandial lipaemia in patients with NIDDM

Overproduction of intestinal lipoprotein containing apolipoprotein B-48 in Psammomys obesus: impact of dietary n-3 fatty acids

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