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Interesterification rearranges the position of fatty acids within triacylglycerols, the main component of dietary fat, altering physical properties such as the melting point and providing suitable functionality for use in a range of food applications. Interesterified (IE) fats are one of a number of alternatives which have been adopted to reformulate products to remove fats containing trans fatty acids generated during partial hydrogenation, which are known to be detrimental to cardiovascular health. The use of IE fats can also reduce the saturated fatty acid (SFA) content of the final product (e.g. up to 20% in spreads), while maintaining suitable physical properties (e.g. melt profile). A novel analysis was presented during the roundtable which combined data from the UK National Diet and Nutrition Survey (2012/2013–2013/2014) with expert industry knowledge of the IE fats typically used in food products, to provide the first known estimate of population intakes of IE fats among UK children and adults. IE fats were found to contribute approximately 1% of daily energy across all ages. The major contributors to overall IE fat intakes were fat spreads (~54%) and bakery products (~22%), as well as biscuits (~8%), dairy cream alternatives (~6%) and confectionery (~6%). Increasing use of IE fats could contribute towards reducing total SFA intakes in the population, but would depend on which food products were reformulated and their frequency of consumption among sub‐groups of the population. Studies comparing the effect of IE and non‐IE fats on markers of lipid metabolism have not shown any consistent differences, either in the fasted or in the postprandial state, suggesting a neutral effect of IE fats on cardiovascular disease risk. However, these studies did not use the type of IE fats present in the food supply. This issue has been addressed in two studies by King's College London, which measured the postprandial response to a commercially relevant palm stearin/palm kernel (80:20) IE 'hard stock', although again no consistent effects of the IE fat on markers of lipid metabolism were found. Another study is currently investigating the same IE hard stock, consumed as a fat spread (blended with vegetable oil), and will measure a broader range of postprandial cardiometabolic risk factors. However, further long‐term trials using commercially relevant IE fats are needed. Subsequent to the roundtable, a consumer survey of UK adults (n = 2062; aged 18+ years) suggested that there is confusion about the health effects of dietary fats/fatty acids, including trans fats and partially hydrogenated fats. This may indicate that providing evidence‐based information to the public on dietary fats and health could be helpful, including the reformulation efforts of food producers and retailers to improve the fatty acid profile of some commonly consumed foods. [ABSTRACT FROM AUTHOR]

Obesity and insulin resistance are associated with low-grade systemic inflammation, which is related to increased concentrations of plasma FFAs, glucose, or insulin. Prolonged fasting induces insulin resistance due to elevated plasma FFAs, but is not accompanied by hyperinsulinemia or hyperglycemia. This makes it possible to study effects of physiologically increased FFA concentrations on inflammatory markers, when insulin and glucose concentrations are not increased. In random order, 10 healthy young lean men (mean BMI: 22.8 kg/m2 ) were fasted or fed in energy balance for 60 h with a 2-week wash-out period. Subjects stayed in a respiration chamber during the 60-h periods. Blood samples were taken after 12, 36, and 60 h. Then, a hyperinsulinemic- euglycemic clamp was performed. Fasting decreased insulin sensitivity by 45 % and increased FFA concentrations 5-fold. Fasting did not change concentrations of the inflammatory cytokines TNF-α, IL-1β, IL-6 and IL-8, or of hs- CRP. Effects on vascular endothelial growth factor (VEGF) - which may positively relate to insulin resistance, and on chemerin and leptin - adipokines related to obesity, and obesity-related pathologies, were also studied. At t = 60 h, VEGF concentrations were significantly increased during the fasted period (p < 0.05). At the same time point, chemerin (p < 0.01) and leptin (p < 0.01) were significantly decreased after fasting. For leptin, this decrease was also significant after 36 h (p < 0.01). Adiponectin levels remained unchanged. In healthy young lean men, fastinginduced increases in FFAs leading to insulin resistance do not cause changes in concentrations of the inflammatory cytokines. VEGF concentrations increased and those of chemerin decreased. [ABSTRACT FROM AUTHOR]

Introduction:Mushrooms are known for their immune modulating effect for which the polysaccharide fraction, mainly glucans, seem to be responsible. Fungal β-glucans have been studied extensively, whereas little is known about mushroom α-glucans. We have earlier shown that the polysaccharide fraction from the mushroom A. bisporus, consisting 90% of α-glucans, induced in vitro tumor necrosis factor (TNF)α and nitric oxide production. The purpose of this study was to evaluate the effects of consuming.Method:A. bisporus α-glucan on ex vivo cytokine production by human peripheral mononuclear blood cells (PBMCs). A double-blind randomized trial was designed in which 56 mildly hypercholesterolemic subjects consumed a control fruit juice with no added α-glucans (200 ml/day) for a 2-week run-in period. For the next 5 weeks, the control group (N=30) continued consumption of the control fruit juice, whereas the intervention group (N=26) consumed the same fruit juice enriched with α-glucans from A. bisporus (5 g glucans/day). Changes in interleukin (IL)-1β, IL-6 and TNFα cytokine production by lipopolysaccharide (LPS)-stimulated PBMCs were evaluated, as well as changes in T-helper (Th)1/Th2 cytokines by phytohemaggutinin (PHA)-stimulated PBMCs.Results:Consumption of A. bisporus α-glucans lower LPS-induced TNFα production by 69% (P=0.017) as compared with the control group, whereas no effect on IL-1β and IL-6 was observed. No obvious Th1–Th2 skewing by PHA-stimulated PBMCs was observed. However, we observed a trend towards a decreased production of IL-12 and IL-10.Conclusion:Our current finding suggests that in vivo, α-glucans have lost their efficacy to stimulate the immune response as observed in our in vitro mouse model. [ABSTRACT FROM AUTHOR]

Objective: To collect (i) baseline data and (ii) execute a large multicentre study examining the effect of trans alpha-linolenic acid on its incorporation into plasma lipids and on risk factors for coronary heart disease.Design: Male volunteers were recruited and the habitual diet assessed by a 4-d weighed record. Fatty acid composition of plasma and platelet lipids were determined by gas chromatography at baseline. After a 6 week run-in period on a trans 'free' diet, male volunteers were randomised to consume 0.6 % of energy trans alpha-linolenic acid or to continue with a diet 'low' in trans alpha-linolenic acid for 6 weeks.Setting: Three European university research departments supported by the research and development departments of the food industry.Subjects: Male volunteers (88) recruited by local advertisement.Methods: Replacement of 30 % of the fat of the habitual diet by margarine, oil and foods. Rapeseed oil was deodorised especially to produce the trans 'free' and 'high' trans foods for this study. The incorporation and conversion of trans alpha-linolenic acid into plasma lipids and platelets was assessed by gas chromatography and dietary compliance was verified by 4-d weighed record.Results: Less trans alpha-linolenic acid isomers are incorporated into human plasma lipids in French volunteers than in Dutch or Scottish volunteers consuming their habitual diets. Trans 'free' alpha-linolenic acid-rich oil can be produced by careful deodorization during refining. The 'high' trans diet provided 1410+/-42 mg/d trans isomers of alpha-linolenic acid, whilst the 'low' trans group consumed 60+/-75 mg/d. The change in plasma lipid and platelet fatty acid composition documented that trans linolenic isomers are incorporated and converted to a trans isomer of eicosapentaenoic acid. Only the 15-trans alpha-linolenic acid is incorporated into plasma cholesteryl esters. The group consuming low trans diet had a slightly higher intake of fat, especially saturated and monounsaturated fat.Conclusions: Trans 'free' rapeseed oil, rich in alpha-linolenic acid, can be produced by careful deodorization. Dietary records show good compliance. Dietary trans isomers of alpha-linolenic acid are incorporated in plasma lipids and converted to long-chain polyunsaturated fatty acids. Their effects on risk factors for coronary heart disease and their metabolism will be reported elsewhere.Sponsorship: European Commission (FAIR 95-0594 grant). European Journal of Clinical Nutrition (2000) 54, 104-113 [ABSTRACT FROM AUTHOR]

In the present intervention study we compared the effects of α-linolenic acid with those of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on platelet aggregation in vitro and ex vivo in healthy non-institutionalized elderly subjects. We also compared the effects of α-linolenic acid on platelet aggregation in elderly subjects with those in younger volunteers. During a run-in period of 3 weeks all subjects (thirty-eight elderly (> 60 years) and twelve younger volunteers (< 35 years)) received a diet rich in oleic acid. For the next 6 weeks the elderly subjects received a diet rich in oleic acid (n 11), α-linolenic acid (n 14) (6·8 g/d) or EPA/DHA (n 13) (1·05 g EPA plus 0·55 g DHA). The younger subjects were given a diet rich in α-linolenic acid. The diets did not affect ADP- or collagen-induced platelet aggregation in vitro in either platelet-rich plasma or whole blood. The ex vivo platelet aggregation as measured with filtragometry was significantly decreased in the elderly group that received EPA/DHA compared with the α-linolenic acid (P = 0·006) and the oleic acid (P = 0·005) diet groups. Effects of α-linolenic acid were not age-dependent. Our results suggest that α-linolenic acid and EPA/DHA do not change in vitro platelet aggregation. Compared with oleic acid, EPA/DHA, but not α-linolenic acid, favourably affects ex vivo platelet aggregation in healthy elderly subjects. [ABSTRACT FROM PUBLISHER]

Objective: Our purpose was to investigate whether plasma lipid-soluble antioxidant levels during the third trimester of pregnancy and immediately after birth are altered in women with pregnancy-induced hypertension.Design: Nested case-control study of women with pregnancy-induced hypertension.Subjects: A group of 23 women with (mild) pregnancy-induced hypertension and their neonates, were compared with 23 matched controls with uncomplicated pregnancies.Methods: Concentrations of vitamin E isomers, several carotenoids, and retinol were determined by HPLC in venous plasma which had been stored for 2-5 y. Antioxidant levels were adjusted for the degree of fatty acid unsaturation in plasma phospholipids as analysed 2-5 y before.Results: In the third trimester of pregnancy, lipid-soluble antioxidant levels were similar in women with pregnancy-induced hypertension and controls. From the third trimester to postpartum, mean (+/- s.e.m.) beta + gamma-tocopherol levels decreased by 0.38 +/- 0.17 mumol/l or 5% (P = 0.038) in the control group. In the pregnancy-induced hypertension group, however, plasma levels of most antioxidants decreased from the third trimester to postpartum, but only the decreases in plasma levels of beta + gamma-tocopherol of 1.08 +/- 0.27 mumol/l or 26% (P = 0.042), of alpha-tocopherol of 2.51 +/- 1.58 mumol/l or 6% (P = 0.024), and of lutein of 0.13 +/- 0.04 mumol/l or 15% (P = 0.013) reached statistical significance as compared with the changes in the control group. At the same time, the polyunsaturated fatty acid unsaturation index of plasma phospholipids (UI) decreased in the pregnancy-induced hypertension group as well. Consequently, antioxidant levels, adjusted for UI, changed similarly in both groups. Umbilical vein plasma antioxidant levels were also similar after complicated and uncomplicated pregnancies.Conclusion: Plasma lipid-soluble antioxidant levels in mother and child are affected by mild pregnancy-induced hypertension, but this effect disappears after adjustment for fatty acid unsaturation. [ABSTRACT FROM AUTHOR]

Conclusion We conclude that13C α-linolenic acid is converted into its LCP. The conversion of α-linolenic acid into its LCP appears to be inhibited on diets rich in EPA/DHA, while it appears not to be influenced by age. In addition, oxidation of α-linolenic acid is not dependent on age or dietary α-linolenic acid, but may be slightly increased on diets rich in EPA/DHA. [ABSTRACT FROM AUTHOR]

Cardiovascular disease has a multifactorial aetiology, as is illustrated by the existence of numerous risk indicators, many of which can be influenced by dietary means. It should be recalled, however, that only after a cause-and-effect relationship has been established between the disease and a given risk indicator (called a risk factor in that case), can modifying this factor be expected to affect disease morbidity and mortality. In this paper, effects of diet on cardiovascular risk are reviewed, with special emphasis on modification of the plasma lipoprotein profile and of hypertension. In addition, dietary influences on arterial thrombotic processes, immunological interactions, insulin resistance and hyperhomocysteinaemia are discussed. Diet-ary lipids are able to affect lipoprotein metabolism in a significant way, thereby modifying the risk of cardiovascular disease. However, more research is required concerning the possible interactions between the various dietary fatty acids, and between fatty acids and dietary cholesterol. In addition, more studies are needed with respect to the possible importance of the postprandial state. Although in the aetiology of hypertension the genetic component is definitely stronger than environmental factors, some benefit in terms of the development and coronary complications of atherosclerosis in hypertensive patients can be expected from fatty acids such as α-linolenic acid, eicosapentaenoic acid and docosahexaenoic acid. This particularly holds for those subjects where the hypertensive mechanism involves the formation of thromboxane A2 and/or α1-adrenergic activities. However, large-scale trials are required to test this contention. Certain aspects of blood platelet function, blood coagulability, and fibrinolytic activity are associated with cardiovascular risk, but causality has been insufficiently proven. Nonetheless, well-designed intervention studies should be initiated to further evaluate such promising dietary components as the various n−3 and n−6 fatty acids and their combination, antioxidants, fibre, etc. for their effect on processes participating in arterial thrombus formation. Long-chain polyenes of the n−3 family and antioxidants can modify the activity of immunocompetent cells, but we are at an early stage of examining the role of immune function on the development of atherosclerotic plaques. Actually, there is little, if any, evidence that dietary modulation of immune system responses of cells participating in atherogenesis exerts beneficial effects. Although it seems feasible to modulate insulin sensitivity and subsequent cardiovascular risk factors by decreasing the total amount of dietary fat and increasing the proportion of polyunsaturated fatty acids, additional studies on the efficacy of specific fatty acids, dietary fibre, and low-energy diets, as well as on the mechanisms involved are required to understand the real function of these dietary components. Finally, dietary supplements containing folate and vitamins B6 and/or B12 should be tested for their potential to reduce cardiovascular risk by lowering the plasma level of homocysteine. [ABSTRACT FROM PUBLISHER]

We evaluated oxyphytosterol (OPS) concentrations in plasma and various tissues of two genetically modified mouse models with either increased cholesterol (apoE KO mice) or increased cholesterol and plant sterol (PS) concentrations (apoExABCG8 dKO mice). Sixteen female apoE KO and 16 dKO mice followed the same standard, low OPS-chow diet. Animals were euthanized at 36 weeks to measure PS and OPS concentrations in plasma, brain, liver and aortic tissue. Cholesterol and oxysterol (OS) concentrations were analyzed as reference for sterol oxidation in general. Plasma campesterol (24.1 ± 4.3 vs. 11.8 ± 3.0 mg/dL) and sitosterol (67.4 ± 12.7 vs. 4.9 ± 1.1 mg/dL) concentrations were severely elevated in the dKO compared to the apoE KO mice (p < 0.001). Also, in aortic and brain tissue, PS levels were significantly elevated in dKO. However, plasma, aortic and brain OPS concentrations were comparable or even lower in the dKO mice. In contrast, in liver tissue, both PS and OPS concentrations were severely elevated in the dKO compared to apoE KO mice (sum OPS: 7.4 ± 1.6 vs. 4.1 ± 0.8 ng/mg, p < 0.001). OS concentrations followed cholesterol concentrations in plasma and all tissues suggesting ubiquitous oxidation. Despite severely elevated PS concentrations, OPS concentrations were only elevated in liver tissue, suggesting that OPS are primarily formed in the liver and plasma concentrations originate from hepatic spill-over into the circulation., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Dietary plant sterols and stanols as present in our diet and in functional foods are well-known for their inhibitory effects on intestinal cholesterol absorption, which translates into lower low-density lipoprotein cholesterol concentrations. However, emerging evidence suggests that plant sterols and stanols have numerous additional health effects, which are largely unnoticed in the current scientific literature. Therefore, in this review we pose the intriguing question "What would have occurred if plant sterols and stanols had been discovered and embraced by disciplines such as immunology, hepatology, pulmonology or gastroenterology before being positioned as cholesterol-lowering molecules?" What would then have been the main benefits and fields of application of plant sterols and stanols today? We here discuss potential effects ranging from its presence and function intrauterine and in breast milk towards a potential role in the development of non-alcoholic steatohepatitis (NASH), cardiovascular disease (CVD), inflammatory bowel diseases (IBD) and allergic asthma. Interestingly, effects clearly depend on the route of entrance as observed in intestinal-failure associated liver disease (IFALD) during parenteral nutrition regimens. It is only until recently that effects beyond lowering of cholesterol concentrations are being explored systematically. Thus, there is a clear need to understand the full health effects of plant sterols and stanols., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background and Aims: Earlier studies in our group suggested that traditionally prepared buttermilk influences cholesterol metabolism. We therefore designed a study to evaluate whether traditionally prepared buttermilk lowers serum low-density lipoprotein cholesterol (LDL-C) and/or prevents the LDL-C raising effect of egg yolks., Methods and Results: Mildly hypercholesterolemic subjects were randomly allocated to one of four diet groups consuming daily at lunch 80 ml skimmed milk with (n = 23) or without (n = 25) lutein-enriched egg yolk (28 g from 1.5 eggs providing 323 mg cholesterol) or traditionally prepared buttermilk with (n = 23) or without (n = 21) lutein-enriched egg yolk during a 12 week period. Fasting blood samples were taken to measure concentrations of serum lipids, (apo)lipoproteins, liver and kidney function markers, and plasma lutein, zeaxanthin and high-sensitive C-reactive protein (hsCRP). Egg yolk consumption significantly increased serum total cholesterol (total-C) (p = 0.035) and LDL-C concentrations (p = 0.022). Buttermilk did not change the effects of egg yolk on serum lipids and (apo)lipoproteins. There was a trend towards significant lower total-C (p = 0.077), but not LDL-C (p = 0.204) concentrations in the buttermilk groups. Plasma lutein and zeaxanthin concentrations increased significantly (p < 0.001) in the egg yolk groups., Conclusion: In mildly hypercholesterolemic subjects, daily consumption of traditionally prepared buttermilk for 12 weeks did not lower serum total-C or LDL-C concentrations, nor did it prevent the serum total-C and LDL-C raising effect of daily egg yolk consumption., Registration Number: This study is registered at www.clinicaltrials.gov as NCT01566305., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Background and Aims: To compare the effects of n-3 long chain polyunsaturated fatty acids (n-3 LCPUFA), with those of fenofibrate, on markers of inflammation and vascular function, and on the serum lipoprotein profile in overweight and obese subjects., Methods and Results: Twenty overweight and obese subjects participated in a randomized, double-blind, placebo-controlled intervention trial and received 3.7 g/d n-3 fatty acids (providing 1.7 g/d EPA and 1.2 g/d DHA), 200 mg fenofibrate or placebo treatment for 6 weeks separated by a 2 weeks wash-out period. Fish oil and fenofibrate treatment reduced triglyceride (-0.61 ± 0.81 mmol/L, P < 0.001, and -0.34 ± 0.85 mmol/L, P = 0.048, respectively) and increased HDL cholesterol concentrations (0.13 ± 0.21 mmol/L, P = 0.013, and 0.10 ± 0.18 mmol/L, P = 0.076), as reflected by a decrease of large very VLDL particles and increases of large HDL particles and medium size HDL particles. Fish oil increased serum LDL cholesterol concentrations (0.34 ± 0.59 mmol/L, P = 0.013). Fenofibrate reduced concentrations of soluble endothelial selectin (sE-selectin) (-4.1 ± 7.5 ng/mL, P = 0.032), but increased those of macrophage chemoattractant protein 1 (MCP1) (28 ± 55 ng/mL, P = 0.034). Fish oil had no effects on these markers., Conclusion: Although n-3 LCPUFA and fenofibrate can both activate PPARα, they have differential effects on cardiovascular risk markers. In overweight and obese subjects fenofibrate (200 mg/d) or n-3 LCPUFA (3.7 g/d) treatment for 6 weeks did not improve markers for low-grade systemic inflammation, while fenofibrate had more profound effects on plasma lipids and markers for vascular activity compared to fish oil. Registration number clinical trials EudraCT 2006-005743-28., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Background and Aims: Epidemiological studies have indicated a negative relation between low-fat dairy consumption and the metabolic syndrome. However, evidence from intervention studies is scarce. Our aim was to investigate the effects of daily consumption of low-fat dairy products on metabolic risk parameters in overweight and obese men and women., Methods and Results: Thirty-five healthy subjects (BMI>27 kg/m(2)) consumed low-fat dairy products (500 mL low-fat milk and 150 g low-fat yogurt) or carbohydrate-rich control products (600 mL fruit juice and 3 fruit biscuits) daily for 8 weeks in random order. Compared with the control period, systolic blood pressure was decreased by 2.9 mm Hg (95% confidence interval (CI), -5.5 to -0.3 mm Hg; P=0.027), while the difference in diastolic blood pressure did not reach statistical significance (95% CI, -3.4 to 0.3 mm Hg; P=0.090). Low-fat dairy consumption decreased HDL-cholesterol concentrations by 0.04 mmol/L (95% CI, -0.07 to -0.01 mmol/L; P=0.021) and apo A-1 concentrations by 0.04 g/L (95% CI, -0.07 to -0.01 g/L; P=0.016) compared with control. Serum total cholesterol, LDL-cholesterol, apo B, triacylglycerols, non-esterified fatty acids, glucose, insulin, C-reactive protein and plasminogen activator inhibitor-1 were unchanged., Conclusion: We conclude that in overweight and obese subjects, daily intake of low-fat dairy products for 8 weeks decreased systolic blood pressure, but did not improve other metabolic risk factors related to the metabolic syndrome., (Copyright © 2009 Elsevier B.V. All rights reserved.)

Microarray technology allows us to perform high-throughput screening of changes in gene expression. The outcome of microarray experiments largely depends on the applied analysis methods and cut-off values chosen. Results are often required to be verified using a more sensitive detection technique, such as quantitative real-time PCR (qPCR or RT-PCR). Throughout the years, this technique has become a de facto golden standard. Individual qPCRs are time-consuming, but the technology to perform high-throughput qPCR reactions has become available through PCR-arrays that allow up to 384 PCR reactions simultaneously. Our current aim was to investigate the usability of a RT(2) Profilertrade mark PCR-array as validation in a nutritional intervention study, where the measured changes in gene expression were low. For some differentially expressed genes, the PCR-array confirmed the microarray prediction, though not for all. Furthermore, the PCR-array allowed picking up the expression of genes that were not measurable on the microarray platform but also vice versa. We conclude that both techniques have their own (dis)advantages and specificities, and for less pronounced changes using both technologies may be useful as complementation rather than validation.

The metabolic syndrome (MS) is a clustering of metabolic abnormalities that increases the risk to develop chronic diseases such as cardiovascular disease and type 2 diabetes mellitus. Although its precise aetiology is unknown, dietary habits play a major role. Nowadays, more and more attention is paid to the glycemic index (GI) and the glycemic load (GL) of a diet. The GI of a food is a value based on the average increase in blood glucose levels occurring when a 50 g carbohydrate portion of that food is consumed. The GL accounts for the amount of carbohydrate per serving. From reviewing the current literature, we conclude that for healthy and/or overweight subjects the importance of low GI or GL diets in relation to the metabolic syndrome has not been established. One of the reasons is that the diets used in the intervention studies frequently not only differed in GI or GL, but also in fibre, protein and/or fat content. In some of the prospective cohort studies, effects of GI or GL attenuated or even disappeared after correcting for fibre intake. This makes it impossible to ascribe the possible beneficial metabolic effects of low GI or GL diets unequivocally to the GI or GL. The question, therefore, remains open on to what components of the metabolic syndrome are specifically affected by the GI per se. To answer this question, controlled longer-term intervention studies are needed to monitor the effects of the GI on the various components of the metabolic syndrome.