Biomedical subjects

Jogchum Plat

Publications and source records attributed to Jogchum Plat.

6 recordsLinked to original sources

PubMed2003

Metabolic effects of plant sterols and stanols (Review).

High serum LDL cholesterol concentration is a major risk factor for cardiovascular complications. This risk can be lowered by diet. In this respect foods containing plant sterol or stanol esters can be useful for mildly- and hypercholesteraemic subjects. Plant sterols and stanols, which are structurally related to cholesterol, decrease the incorporation of dietary and biliary cholesterol into micelles. This lowers cholesterol absorption. Furthermore, these components increase ABC-transporter expression, which may also contribute to the decreased cholesterol absorption. Consequently, cholesterol synthesis and LDL receptor activity increase, which ultimately leads to decreased serum LDL cholesterol concentrations. Animal studies have further shown that these dietary components may also lower atherosclerotic lesion development. Plant sterols and stanols also lower plasma lipid-standardized concentrations of the hydrocarbon carotenoids, but not those of the oxygenated cartenoids and tocopherols. Also, vitamin A and D concentrations are not affected. Although absorption of plant sterols and stanols (0.02-3.5%) is low compared to cholesterol (35-70%), small amounts are found in the circulation and may influence other physiological functions. However, there is no consistent evidence that plant sterols or stanols can change the risk of colon or prostate cancer, or immune status. In conclusion, plant sterols and stanols effectively reduce serum LDL cholesterol and atherosclerotic risk. In addition potential effects of plant sterols and stanols on other metabolic processes remain to be elucidated.

Animals↗

PubMed2003

Changes in serum concentrations of noncholesterol sterols and lipoproteins in healthy subjects do not depend on the ratio of plant sterols to stanols in the diet.

Consumption of plant sterols or stanols increases their respective serum concentrations, whereas plant sterols might reduce serum concentrations of plant stanols and vice versa. This suggests that changes in serum plant sterol and stanol concentrations depend on the ratio of plant sterols to stanols in the diet. To examine this in more detail, healthy men (n = 15) and women (n = 29) consumed in random order for 3 wk 1.5 g/d of plant sterols plus 0.5 g of plant stanols (high sterol margarine), 1 g of each (low sterol margarine) or control margarine. Sterols and stanols were provided as fatty acid esters. Compared with the control period, serum cholesterol-standardized campesterol and sitosterol concentrations increased by 33 (P < 0.001) and 19% (P < 0.002), respectively, during the high sterol period, but by only 20 (P < 0.001) and 11% (P = 0.001), respectively, during the low sterol period. During the high sterol period, these values for campestanol and sitostanol were 18 (P = 0.063) and 1% (P = 0.630), and during the low sterol period 25 (P = 0.105) and 7% (P = 0.163), respectively. Effects on LDL cholesterol were similar. We therefore conclude that changes in serum plant sterol and stanol concentrations are not greatly affected by the simultaneous consumption of plant sterols and plant stanols, but are proportional to intakes. Furthermore, both mixtures were equally effective in lowering serum LDL cholesterol concentrations.

Adolescent↗

PubMed2002

Effects of plant stanol esters supplied in low-fat yoghurt on serum lipids and lipoproteins, non-cholesterol sterols and fat soluble antioxidant concentrations.

Oil-based products enriched with plant stanol esters can lower low-density lipoprotein (LDL) cholesterol concentrations by 10-14%. Effectiveness of low-fat products, however, has never been evaluated, although such products fit into a healthy diet. We therefore examined the effects of plant stanol esters emulsified into low-fat yoghurt (0.7% fat) on fasting concentrations of plasma lipids and lipid-soluble antioxidants, which may also change by plant stanol consumption. Sixty non-hypercholesterolemic subjects first consumed daily three cups (3 x 150 ml) of placebo yoghurt for 3 weeks. For the next 4 weeks, 30 subjects continued with the placebo yoghurt, while the other 30 subjects received three cups of experimental yoghurt. Each cup provided 1 g of plant stanols (0.71 g sitostanol plus 0.29 g campestanol) as its fatty acid ester. LDL cholesterol (mean+/-S.D.) increased by 0.06+/-0.21 mmol/l in the placebo group, but decreased by -0.34+/-0.30 mmol/l in the experimental group. The difference in changes between the two groups of 0.40 mmol or 13.7% was highly significant (P<0.001; 95% confidence interval for the difference, (-)0.26 -(-)0.53 mmol/l). Effects were already maximal after 1 week. HDL cholesterol and triacylglycerol concentrations did not change. Total tocopherol levels increased by 1.43 micromol/mmol LDL cholesterol (14.0%, P=0.015). beta-carotene levels, however, decreased by -0.02 micromol/mmol LDL cholesterol (-14.4%, P=0.038). Decreases in absolute beta-carotene concentrations were found in all apoB-containing lipoproteins. LDL-cholesterol standardised phytofluene levels decreased by 21.4+/-25.7% (P<0.001), while other plasma carotenoid (lutein/zeaxanthin, beta-cryptoxanthin, lycopene and alpha-carotene) levels did not change significantly. We conclude that low-fat yoghurt enriched with plant stanol esters lowers within 1 week LDL cholesterol to the same extent as oil-based products. LDL-cholesterol standardised concentrations of tocopherol increased. The observed decrease in beta-carotene levels, as found in many other studies, appears not to be limited to the LDL fraction.

Adolescent↗

PubMed2002

Post-genomic opportunities for understanding nutrition: the nutritionist's perspective.

Until 15-20 years ago, many nutritionists were mainly interested in the effects of diet on health-related variables such as blood pressure and serum cholesterol concentrations. Without doubt, these studies have made an important contribution to our current understanding of the relationship between diet and health. For many reasons, however, few researchers have tried to explain these effects at the molecular level. Nowadays, however, it seems that the picture has been reversed; much research is being directed towards studying the effects of dietary components at the molecular level. This type of research has been made possible by, among other factors, the implementation of techniques from the more fundamental sciences into nutrition research. Also, the availability of genome sequences has accelerated this shift of interest. The aims of these studies are to obtain detailed information on the molecular and metabolic responses of cells and tissues, or even the whole organism, to dietary components. In these studies, also, the interactions between diet and genetic background, and between diet and different physiological and pathological conditions need to be addressed. However, it is not only important to obtain information on mechanisms, but also on the functional consequences for the organism. One ultimate question, however, is whether this information can be used to develop tests that can form the basis of dietary advice for specific subpopulations. These challenging questions can only be tackled through an integrated approach that combines the expertise from various disciplines.

Animals↗

PubMed2002

Increased intestinal ABCA1 expression contributes to the decrease in cholesterol absorption after plant stanol consumption.

The hypocholesterolemic effect of plant stanols is explained by a decreased intestinal cholesterol absorption due to a competition between plant stanols and cholesterol for incorporation into mixed micelles. Earlier we had suggested that plant stanols have a so far unknown action inside the enterocytes. The recent discovery of the involvement of ATP binding cassette (ABC) transporters in cholesterol absorption was a lead to further explore the hypocholesterolemic mechanism of plant stanols. We found that mixed micelles enriched with sitostanol or with cholesterol plus sitostanol were potent inducers of ABCA1 expression in caco-2 cells, an accepted model to study human intestinal lipoprotein metabolism. Based on these findings, we now hypothesize that plant stanols--and possibly plant sterols--increase ABCA1-mediated cholesterol efflux back into the intestinal lumen. We further hypothesize that intracellular levels of plant stanols are monitored by the same sensors (SREBP-2 and LXR) as those that monitor cholesterol. Consequently, increased plant stanol levels within the enterocyte activate cholesterol efflux through ABCA1- but not SREBP-2-mediated endogenous cholesterol synthesis even if intracellular cholesterol concentrations are lowered through consumption of plant stanols. If our hypothesis is correct, then the LXR pathway may be a target for dietary regulation of intestinal lipid metabolism.

ATP Binding Cassette Transporter 1↗

PubMed2001

Effects of plant stanol esters on LDL receptor protein expression and on LDL receptor and HMG-CoA reductase mRNA expression in mononuclear blood cells of healthy men and women.

Functional foods enriched with plant stanols lower atherogenic LDL cholesterol concentrations. This effect is caused at least partly by a decreased intestinal cholesterol absorption. It has been suggested that LDL production is reduced after plant stanol consumption, but it is unknown whether LDL receptor expression is affected and contributes to the LDL-lowering effect of plant stanols. Markers for endogenous cholesterol synthesis (lathosterol) increase, but it is not known how this higher cholesterol synthesis is regulated at the molecular level. In a double-blind placebo controlled trial, we have found that compared with the control group (N=15), daily consumption of 3.8-4.0 g plant stanol esters (N=29) for 8 weeks increased LDL receptor mRNA levels in human mononuclear blood cells by 43% (P=0.003). LDL receptor protein concentrations on the surface of monocytes and T lymphocytes increased by 37% (P=0.003) and 25% (P=0.013), suggesting an increased translation. This increased protein expression appeared to be functional, since changes in serum LDL cholesterol correlated negatively with changes in LDL receptor mRNA levels (r=-0.361; P=0.015) and changes in LDL receptor protein expression in monocytes (r=-0.440; P<0.001) and T lymphocytes (r=-0.307; P=0.018). Based on these results, we suggest that the higher LDL receptor expression contributed to a lowered LDL formation along the apoB cascade. Whole body cholesterol synthesis increased, as indicated by the rise in serum cholesterol-standardized lathosterol concentrations, but the 34% increased HMG-CoA reductase mRNA concentrations did not reach statistical significance. Nor did it correlate significantly with changes in serum cholesterol-standardized lathosterol concentrations. This suggests that HMG-CoA reductase may be only partly regulated at a transcriptional level.

Cholesterol↗