Biomedical subjects

Ronald P Mensink

Publications and source records attributed to Ronald P Mensink.

At least 19 recordsLinked to original sources

PubMed2007

Fecal water from ileostomic patients consuming oat beta-glucan enhances immune responses in enterocytes.

Yeast, fungal, and dietary beta-glucans have immune-modulating effects in vitro and in vivo, as thought, mainly by affecting leukocytes; however, effects of oat beta-glucan on enterocytes have never been studied. As recognized, supplying oat beta-glucans as such to cells in culture directly is difficult because of solubility problems. Therefore, six ileostomic patients consumed, in random order, a control diet or an oat beta-glucan enriched diet (5 g) and from the collected ileostomic content, fecal water was prepared and added to two small intestinal cell lines (INT407, Caco-2) and two colon cell lines (HT29, T84) together with a cytokine cocktail (IL-1beta + INFgamma + TNFalpha). Several parameters reflecting immune-modulation were measured. As compared to placebo fecal water, beta-glucan enriched fecal water significantly increased IL-8 production in HT29 (5.0%; p = 0.046) and INT407 cells (22.0%; p = 0.028). Intercellular adhesion molecule (ICAM)-1 expression increased in T84 (11.0%; p = 0.028) and Caco-2 cells (20.4%; p = 0.075). These immune-stimulating effects were confirmed by enhancement of inflammatory expression profiles, as determined with an antibody array. Our findings show immune enhancement by fecal water from ileostomic patients consuming oat beta-glucan both in small intestinal and colon cell lines after stimulation, which is in agreement with documented effects in leukocytes. Whether these immune-stimulating effects on enterocytes contribute to the enhanced protection of the host against invading pathogens as observed both in animals and in humans, as well as the underlying mechanism, needs further evaluation.

Adjuvants, Immunologic↗

PubMed2006

Plant sterol or stanol esters retard lesion formation in LDL receptor-deficient mice independent of changes in serum plant sterols.

Statins do not always decrease coronary heart disease mortality, which was speculated based on increased serum plant sterols observed during statin treatment. To evaluate plant sterol atherogenicity, we fed low density lipoprotein-receptor deficient (LDLr(+/-)) mice for 35 weeks with Western diets (control) alone or enriched with atorvastatin or atorvastatin plus plant sterols or stanols. Atorvastatin decreased serum cholesterol by 22% and lesion area by 57%. Adding plant sterols or stanols to atorvastatin decreased serum cholesterol by 39% and 41%. Cholesterol-standardized serum plant sterol concentrations increased by 4- to 11-fold during sterol plus atorvastatin treatment versus stanol plus atorvastatin treatment. However, lesion size decreased similarly in the sterol plus atorvastatin (-99% vs. control) and the stanol plus atorvastatin (-98%) groups, with comparable serum cholesterol levels, suggesting that increased plant sterol concentrations are not atherogenic. Our second study confirms this conclusion. Compared with lesions after a 33 week atherogenic period, lesion size further increased in controls (+97%) during 12 more weeks on the diet, whereas 12 weeks with the addition of plant sterols or stanols decreased lesion size (66% and 64%). These findings indicate that in LDLr(+/-) mice 1) increased cholesterol-standardized serum plant sterol concentrations are not atherogenic, 2) adding plant sterols/stanols to atorvastatin further inhibits lesion formation, and 3) plant sterols/stanols inhibit the progression or even induce the regression of existing lesions.

Animals↗

PubMed2006

Rationale and design of the TRANSFACT project phase I: a study to assess the effect of the two different dietary sources of trans fatty acids on cardiovascular risk factors in humans.

BACKGROUND: Detrimental effects of consumption of industrial trans fatty acids (TFA) from partially hydrogenated vegetable oils (PHVO) on cardiovascular disease (CVD) risk factors are well documented. However, very little information is available on the effect of natural sources of TFA coming from milk fat, dairy products and ruminant meat. In fact, due to the naturally low level of TFA in milk fat, it is almost impossible to conduct a clinical trial with a limited number of subjects (<200). METHODOLOGY: To compare the effects of industrial and natural dietary sources of TFA, two specific test fats have been designed and produced. A substantial amount of milk fat (130 kg) enriched in TFA has been produced by modification of the cow's diet and selection of cows with the highest TFA content. The level obtained was approximately 4- to 7-fold higher than typically present in milk fat (approximately 20 instead of 3-6 g/100 g of total fatty acids). The control fat is composed of PHVO balanced in saturated fatty acids (lauric, myristic and palmitic). Both experimental fats contain about 20-22% of monounsaturated TFA and the volunteers' daily experimental fat intake (54 g), will represent about 12.0 g/day of TFA or 5.4% of the daily energy (based on 2000 kcal/day). These two test fats have been incorporated into food items and will be provided to 46 healthy subjects under a randomised, double blind, controlled, cross-over design. The primary outcome is high-density lipoprotein cholesterol (HDL-C), which is an independent risk factor for CVD. Other parameters such as low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), and HDL-C level and subclasses will be also to be evaluated. CONCLUSION: We have shown that it is technically feasible to perform a clinical trial on the comparative effects of natural and industrial sources of TFA isomers on CVD risk factors. Results are expected by mid-2006.

Adult↗

PubMed2006

Beta-glucan incorporated into a fruit drink effectively lowers serum LDL-cholesterol concentrations.

BACKGROUND: beta-Glucan can reduce serum concentrations of total and LDL cholesterol. The mechanism of this action is not clear, however, and it is difficult to predict the cholesterol-lowering effect of a food product enriched with beta-glucan. OBJECTIVES: We examined the effects of a beta-glucan-enriched fruit juice on serum lipids and lipoproteins and on markers of cholesterol absorption (serum concentrations of plant sterols) and synthesis (serum concentrations of lathosterol). In addition, we measured effects on lipid-soluble antioxidants. DESIGN: After a 3-wk run-in period, healthy subjects consumed daily a fruit drink providing 5 g rice starch [placebo (control) group; n = 22] or beta-glucan from oats (n = 25) for 5 wk (parallel design). At the end of the run-in period and at the end of the intervention, blood samples were taken for analysis of lipids and lipoproteins, noncholesterol sterols, and fat-soluble antioxidants. Changes between the end of the run-in period and the end of the intervention were calculated for each subject. Differences in changes between the groups were analyzed statistically. RESULTS: The differences between the control and beta-glucan groups in the change in serum concentrations of total and LDL cholesterol, respectively, were -4.8% (P = 0.012) and -7.7% (P = 0.005). The differences between the groups in the change in serum concentrations of lathosterol and sitosterol were -13% (P = 0.023) and -11% (P = 0.030), respectively. No significant effects were found on fat-soluble antioxidants. CONCLUSIONS: Beta-glucan lowers serum concentrations of total and LDL cholesterol when incorporated into a fruit drink. A reduced cholesterol absorption contributes to the cholesterol-lowering effect of beta-glucan without affecting plasma concentrations of lipid-soluble antioxidants.

Adolescent↗

PubMed2006

Conversion of alpha-linolenic acid in humans is influenced by the absolute amounts of alpha-linolenic acid and linoleic acid in the diet and not by their ratio.

BACKGROUND: Human in vivo data on dietary determinants of alpha-linolenic acid (ALA; 18:3n-3) metabolism are scarce. OBJECTIVE: We examined whether intakes of ALA or linoleic acid (LA; 18:2n-6) or their ratio influences ALA metabolism. DESIGN: During 4 wk, 29 subjects received a control diet (7% of energy from LA, 0.4% of energy from ALA, ALA-to-LA ratio = 1:19). For the next 6 wk, a control diet, a low-LA diet (3% of energy from LA, 0.4% of energy from ALA, ratio = 1:7), or a high-ALA diet (7% of energy from LA, 1.1% of energy from ALA, ratio = 1:7) was consumed. Ten days before the end of each dietary period, [U-13C]ALA was administered orally for 9 d. ALA oxidation was determined from breath. Conversion was estimated by using compartmental modeling of [13C]- and [12C]n-3 fatty acid concentrations in fasting plasma phospholipids. RESULTS: Compared with the control group, ALA incorporation into phospholipids increased by 3.6% in the low-LA group (P = 0.012) and decreased by 8.0% in the high-ALA group (P < 0.001). In absolute amounts, it increased by 34.3 mg (P = 0.020) in the low-LA group but hardly changed in the high-ALA group. Nearly all ALA from the plasma phospholipid pool was converted into eicosapentaenoic acid. Conversion of eicosapentaenoic acid into docosapentaenoic acid and docosahexaenoic acid hardly changed in the 3 groups and was <0.1% of dietary ALA. In absolute amounts, it was unchanged in the low-LA group, but increased from 0.7 to 1.9 mg (P = 0.001) in the high-ALA group. ALA oxidation was unchanged by the dietary interventions. CONCLUSION: The amounts of ALA and LA in the diet, but not their ratio, determine ALA conversion.

Breath Tests↗

PubMed2006

Plasma concentrations of plant sterols: physiology and relationship with coronary heart disease.

Recently, it has been questioned whether elevated levels of circulating plant sterols increase the risk of coronary heart disease (CHD). To date, no definitive conclusions regarding such a relationship have been reached, nor have there been any studies summarizing the factors that contribute to the observed elevations in plant sterol concentrations in plasma. Thus, the purpose of this review is to systematically compare the plant sterol levels of subjects from the general population and to describe factors that contribute to the variations observed. The question of whether elevated plasma concentrations of plant sterols are associated with an increased risk of CHD was also assessed. Results indicate that the key factors accounting for variations in circulating plant sterol concentrations include: apolipoprotein E phenotypes, ATP-binding cassette transporter polymorphisms, use of statin drugs, presence of metabolic syndrome, dietary intake of plant sterols, gender, and analytical techniques used in the measurement of plant sterols in the plasma. An analysis of the studies examining the relationship between circulating levels of plant sterols and CHD risk in non-sitosterolemic populations revealed no clear associations. Furthermore, it was shown that the above-mentioned factors play an important role in determining the levels of plant sterols in plasma. Since these factors may act as potential confounders, they must be controlled for before more solid conclusions can be reached.

ATP Binding Cassette Transporter, Subfamily G, Mem↗

PubMed2005

Cis-9, trans- 11 and trans-10, cis-12 conjugated linoleic acid (CLA) do not affect the plasma lipoprotein profile in moderately overweight subjects with LDL phenotype B.

BACKGROUND: Results of a pilot study suggested that cis-9, trans-11 conjugated linoleic acid (CLA) improved LDL phenotype in moderately overweight subjects with LDL phenotype B. OBJECTIVE: Initiated by the results of this pilot study, we have specifically designed a study to test the hypothesis that cis-9, trans-11 conjugated linoleic acid improves LDL phenotype in moderately overweight subjects with LDL phenotype B. Effects on the serum lipid profile, on plasma glucose and insulin concentrations, and on clinical parameters were also examined. DESIGN: Volunteers with LDL phenotype B were divided into three groups consuming daily a drinkable dairy product not enriched with CLA (placebo, n = 34), the same dairy product enriched with 3g c9, t11 CLA (n = 34), or the dairy product enriched with 3g t10, c12 CLA (n = 19) for 13 weeks. RESULTS: Median changes in the proportions of plasma small dense LDL were -2.0% in the control group and -0.1% in the c9, t11 CLA and t10, c12 CLA groups (p = 0.981 for the differences between the groups). c9, t11 CLA or t10, c12 CLA did also not affect serum concentrations of LDL and HDL cholesterol, and of triacylglycerol, and plasma concentrations of glucose and insulin. CONCLUSIONS: In humans with LDL phenotype B, c9, t11 CLA and t10, c12 CLA do not beneficially change risk factors for cardiovascular disease or diabetes.

Adult↗

PubMed2005

Plant sterols and stanols: effects on mixed micellar composition and LXR (target gene) activation.

Plant stanols and sterols of the 4-desmethyl family (e.g., sitostanol and sitosterol) effectively decrease LDL cholesterol concentrations, whereas 4,4-dimethylsterols (alpha-amyrin and lupeol) do not. Serum carotenoid concentrations, however, are decreased by both plant sterol families. The exact mechanisms underlying these effects are not known, although effects on micellar composition have been suggested. With a liver X receptor (LXR) coactivator peptide recruitment assay, we showed that plant sterols and stanols from the 4-desmethylsterol family activated both LXRalpha and LXRbeta, whereas 4,4-dimethyl plant sterols did not. In fully differentiated Caco-2 cells, the functionality of this effect was shown by the increased expression of ABCA1, one of the known LXR target genes expressed by Caco-2 cells in measurable amounts. The LXR-activating potential of the various plant sterols/stanols correlated positively with ABCA1 mRNA expression. Reductions in serum hydrocarbon carotenoids could be explained by the effects of the 4-desmethyl family and 4,4-dimethylsterols on micellar carotenoid incorporation. Our findings indicate that the decreased intestinal absorption of cholesterol and carotenoids by plant sterols and stanols is caused by two distinct mechanisms.

ATP Binding Cassette Transporter 1↗

PubMed2005

Plant stanol and sterol esters in the control of blood cholesterol levels: mechanism and safety aspects.

Incorporation of plant stanol esters into margarine is among the first examples of a functional food with proven low-density lipoprotein (LDL) cholesterol-lowering effectiveness. Recently, there have been many studies on the effects of plant stanols/sterols on cholesterol metabolism. It has been found that the serum LDL cholesterol-lowering effect of plant stanols/sterols originates from reduced intestinal cholesterol absorption, a process in which changes in micellar composition are thought to play a major role. However, recent findings suggest that there is an additional process in which plant stanols/sterols actively influence cellular cholesterol metabolism within intestinal enterocytes. Furthermore, in response to the reduced supply of exogenous cholesterol, receptor-mediated lipoprotein cholesterol uptake is probably enhanced, as shown by increased LDL receptor expression. At recommended intakes of about 2 to 2.5 g/day, products enriched with plant stanol/sterol esters lower plasma LDL cholesterol levels by 10% to 14% without any reported side effects. Thus, plant stanols/sterols can be considered to be effective and safe cholesterol-lowering functional food ingredients.

Cholesterol, LDL↗

PubMed2005

Compartmental modeling to quantify alpha-linolenic acid conversion after longer term intake of multiple tracer boluses.

To estimate in vivo alpha-linolenic acid (ALA; C18:3n-3) conversion, 29 healthy subjects consumed for 28 days a diet providing 7% of energy from linoleic acid (C18:2n-6) and 0.4% from ALA. On day 19, subjects received a single bolus of 30 mg of uniformly labeled [(13)C]ALA and for the next 8 days 10 mg twice daily. Fasting plasma phospholipid concentrations of (12)C- and (13)C-labeled ALA, eicosapentaenoic acid (EPA; C20:5n-3), docosapentaenoic acid (DPA; C22:5n-3), and docosahexaenoic acid (DHA; C22:6n-3) were determined on days 19, 21, 23, 26, 27, and 28. To estimate hepatic conversion of n-3 fatty acids, a tracer model was developed based on the averaged (13)C data of the participants. A similar tracee model was solved using the averaged (12)C values, the kinetic parameters derived from the tracer model, and mean ALA consumption. ALA incorporation into plasma phospholipids was estimated by solving both models simultaneously. It was found that nearly 7% of dietary ALA was incorporated into plasma phospholipids. From this pool, 99.8% was converted into EPA and 1% was converted into DPA and subsequently into DHA. The limited incorporation of dietary ALA into the hepatic phospholipid pool contributes to the low hepatic conversion of ALA into EPA. A low conversion of ALA-derived EPA into DPA might be an additional obstacle for DHA synthesis.

Adult↗

PubMed2005

The plasminogen activator inhibitor-1 (PAI-1) promoter haplotype is related to PAI-1 plasma concentrations in lean individuals.

BACKGROUND: Elevated plasminogen activator inhibitor-1 (PAI-1) concentrations are associated with cardiovascular diseases. PAI-1 antigen levels are influenced by environmental factors such as body mass index (BMI), and by genetic factors. The PAI-1 promoter of the PAI-1 gene contains two common polymorphisms (-844A/G and -675(4G/5G)) and the 4G allele of the -675(4G/5G) variation has been associated with elevated PAI-1 concentrations and on some occasions with an increased risk of cardiovascular disease. OBJECTIVES: The aim of our study was to investigate the effect of the PAI-1 promoter haplotype on PAI-1 concentrations and to determine the role of BMI. METHODS: The association between the PAI-1 promoter haplotype and PAI-1 antigen levels was investigated in two independent populations, each including 600 healthy Caucasians. Furthermore, to assess the effect of the PAI-1 promoter haplotype on PAI-1 promoter activity, in vitro reporter gene assays were performed in HepG2 and BAEC cells. RESULTS: We observed significantly higher PAI-1 concentrations in A-4G homozygotes than in G-5G carriers in lean subjects (BMI in the lowest quartile). In these lean subjects, the PAI-1 concentrations in A-4G/G-5G heterozygotes were reduced to 60-75%, and the concentrations in G-5G homozygotes to 45-55%, compared to the PAI-1 concentrations of A-4G homozygotes (p < 0.01). PAI-1 concentrations increased approximately four-fold from the lowest to the highest BMI quartile (p < 0.01). The reporter gene assays did not support a direct effect of the PAI-1 promoter haplotype on promoter activity in HepG2 or BEAC cells. CONCLUSIONS: Our study suggests that the PAI-1 promoter haplotype and BMI affect PAI-1 concentrations and that BMI is a stronger determinant than PAI-1 promoter variation.

Adult↗

PubMed2005

Effects of specific CLA isomers on plasma fatty acid profile and expression of desaturases in humans.

Human studies suggest that CLA changes metabolism, possibly through effects on mRNA expression of desaturase and elongase enzymes. In this respect, differential effects of the two most common dietary CLA isomers, cis-9,trans-11 (c9,t11) and trans-10,cis-12 (t10,c12) CLA, have hardly been studied. We therefore gave 25 healthy, overweight men and women daily for 6 wk a drinkable dairy product containing 3 g of oil that was rich in oleic acid. For the next 18 wk, the control group (n = 7) continued to use this product, whereas the second (n = 9) and third groups (n = 9) received products with 3 g of purified c9,t11 CLA or t10,c12 CLA. For each gram of c9,t11 CLA consumed, the proportion in plasma phospholipids increased by 0.26%. For t10, c12 CLA, this value was 0.20%. The t10,c12 CLA isomer increased plasma TAG levels of conjugated 18:3, whereas c9,t11 CLA increased those of both conjugated 18:3 and 20:3. In plasma phospholipids, the delta9 desaturation index of 18:0 (18:1 n-9/18:0) was decreased by t10,c12 CLA (P= 0.03 for diet effects), and the delta6 desaturation index [(18:3n-6 + 20:3n-6)/18:2n-6] was decreased by both CLA isomers (P < 0.01 for diet effects). The delta5 desaturation index (20:4n-6/20:3n-6) and the delta9 desaturation index of 16:0 (16:1 n-7/16:0) were not affected. No effects were seen on mRNA expression of desaturases and elongase in peripheral blood mononuclear cells (PBMC). We therefore conclude that incorporation of c9,t11 and t10,c12 CLA into plasma lipids reflects dietary intakes. Compared with oleic acid, delta9 and delta6 desaturation indices in plasma phospholipids are decreased after consumption of c9,t11 or t10,c12 CLA. Effects on desaturation indices were, however, not reflected by changes at the transcriptional level for the various desaturases and elongase enzymes in PBMC.

Adult↗

PubMed2005

Effects of the individual isomers cis-9,trans-11 vs. trans-10,cis-12 of conjugated linoleic acid (CLA) on inflammation parameters in moderately overweight subjects with LDL-phenotype B.

Immune-modulating effects of CLA have been reported in animals, but results are inconsistent. In humans, CLA has shown no effects or only minor effects on immune function. The objective of this study was to evaluate the immune-modulating effects of 3 g cis-9,trans-11 (c9,t11) vs. trans-10,cis-12 (t10,c12) CLA isomers in a population with a high risk of coronary heart disease characterized by moderate overweight (body-mass index, 25-32.5 kg/m2) in combination with LDL-phenotype B (> or = 35% small LDL cholesterol, density > or = 1.040 g/mL). After a run-in period of 1 wk, 42 men and women were randomly allocated to the c9,t11 CLA group, the t10,c12 CLA group, or the placebo group. Effects of 13 wk of consumption of 3 g of CLA isomers on cytokine production by ex vivo lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells (PBMC) and whole blood, and on plasma C-reactive protein (CRP) concentrations were evaluated. To generate hypotheses for future studies, protein expression patterns of 42 cytokines, chemokines, and growth factors were evaluated with an antibody array in pooled, nonstimulated, fasting plasma samples. LPS induced interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha production by PBMC, and whole blood as well as plasma CRP concentrations were not significantly changed by the c9,t11 and the t10,c12 CLA isomers. The cytokine expression profile in nonstimulated plasma suggested that both CLA isomers induced a specific inflammatory signature, in which the c9,t11 CLA group showed more activity in terms of numbers of proteins regulated. We conclude that daily consumption of 3 g of c9,t11 or t10,c12 CLA isomer did not affect LPS-stimulated cytokine production by PBMC or whole blood and plasma CRP levels. Inflammatory signatures in fasting, nonstimulated plasma as determined by an antibody array may indicate enhanced immune function by both CLA isomers.

Adult↗

PubMed2005

Effects of stearic acid on plasma lipid and lipoproteins in humans.

More than 40 years ago, saturated FA with 12, 14, and 16 carbon atoms (lauric acid, myristic acid, and palmitic acid) were demonstrated to be "hypercholesterolemic saturated FA". It was further concluded that the serum total cholesterol level would hardly be changed by isocaloric replacement of stearic acid (18:0) by oleic acid (cis-18:1n-9) or carbohydrates. These earlier studies did not address the effects of the various FA on the serum lipoprotein profile. Later studies found that the hypercholesterolemic saturated FA increase serum total cholesterol levels by raising concentrations of both the atherogenic LDL and the antiatherogenic HDL. Consequently, the ratio of total to HDL cholesterol will hardly change when carbohydrates replace these saturated FA. Compared with other saturated FA, stearic acid lowers LDL cholesterol. Studies on the effects on HDL cholesterol are less conclusive. In some, the effects on HDL cholesterol were comparable to those of palmitic acid, oleic acid, and linoleic acid, whereas in others a decrease was observed. This may suggest that in this respect the source of stearic acid is of importance, which needs however further study. From all these studies, however, it can be concluded that stearic acid may decrease the ratio of total to HDL cholesterol slightly when compared with palmitic or myristic acid. Without doubt, the effects of stearic acid are more favorable than those of trans monounsaturated FA.

Cholesterol, HDL↗

PubMed2005

Small differences in the effects of stearic acid, oleic acid, and linoleic acid on the serum lipoprotein profile of humans.

BACKGROUND: Studies have suggested that oleic and stearic acids, as well as oleic and linoleic acids, have comparable effects on the serum lipoprotein profile. If so, then substituting these three 18-carbon fatty acids for each other would result in similar effects on the serum lipoprotein profile. OBJECTIVE: The aim of this study was to compare simultaneously the effects of stearic, oleic, and linoleic acids on the serum lipoprotein profile of healthy subjects. DESIGN: Forty-five subjects (27 women and 18 men) consumed in random order 3 experimental diets, each for 5 wk. The diets provided 38% of energy from fat, of which 60% was supplied by the experimental fats. The dietary compositions of the diets were the same, except for 7% of energy, which was provided by stearic, oleic, or linoleic acid. At the end of each intervention period, serum lipid and lipoprotein concentrations were measured. In addition, LDL, HDL, and VLDL particle sizes and particle concentrations of lipoprotein subclasses were analyzed by nuclear magnetic resonance spectroscopy. RESULTS: No significant diet-induced changes in serum lipids and lipoproteins were found. Mean (+/-SD) serum LDL-cholesterol concentrations were 3.79 +/- 0.91, 3.71 +/- 0.79, and 3.65 +/- 0.91 mmol/L with the high-stearic acid, high-oleic acid, and high-linoleic acid diets, respectively (P = 0.137 for diet effects). Mean (+/-SD) HDL-cholesterol concentrations were 1.45 +/- 0.43, 1.46 +/- 0.45, and 1.46 +/- 0.44 mmol/L (P = 0.866). LDL, HDL, and VLDL particle sizes and lipoprotein subclass distributions also did not differ significantly between the 3 diets. CONCLUSIONS: With realistic intakes of stearic, oleic, and linoleic acids, differences between their effects on the serum lipoprotein profile are small.

Adult↗

PubMed2005

The dietary alpha-linolenic acid to linoleic acid ratio does not affect the serum lipoprotein profile in humans.

Alpha-linolenic acid [ALA, 18:3(n-3)] and linoleic acid [LA, 18:2(n-6)] have comparable effects on serum lipid and lipoprotein concentrations, but their effects on lipoprotein subclass distributions and particle sizes are unknown. It is also not known whether these effects are changed by the ALA:LA ratio in the diet. To address these questions, healthy subjects (n = 54) consumed a control diet providing 7% of energy (En%) as LA and 0.4 En% as ALA during a 4-wk run-in period. For the following 6 wk of intervention, each diet was consumed by 18 subjects: the control diet, a low-LA diet (3 En% LA, 0.4 En% ALA), or a high-ALA diet (7 En% LA, 1.1 En% ALA). The ALA:LA ratio for the control diet was 1:19 and was 1:7 for the other 2 diets. Compared with the control group, LDL cholesterol decreased significantly in the ALA group (-0.32 mmol/L, P = 0.024), as did total cholesterol, apolipoprotein (apo) B, and the total:HDL cholesterol ratio. None of the dietary interventions affected HDL cholesterol, apo A-1, or triacylglycerol concentrations. The decrease in total VLDL particle concentrations in the low-LA group was due mainly to a decrease in medium VLDL (-16 nmol/L, P = 0.018) and in the high-ALA group to a decrease in small VLDL (-14 nmol/L, P = 0.044). We conclude that the ALA:LA ratio does not affect the serum lipoprotein profile. Compared with the control and LA diets, ALA lowered LDL cholesterol concentrations, possibly caused by the decrease in small VLDL.

Body Weight↗

PubMed2005

Stearic, oleic, and linoleic acids have comparable effects on markers of thrombotic tendency in healthy human subjects.

Because human studies concerning the effects of stearic acid on thrombotic tendency are inconsistent, we compared the effects of stearic acid with those of its unsaturated derivatives, oleic acid and linoleic acid. In this randomized, crossover study, 45 subjects (27 women and 18 men) consumed, in random order, 3 experimental diets, each for 5 wk. Diets contained approximately 38% of energy as fat. Dietary compositions were the same except for 7% of energy from stearic, oleic, or linoleic acids. At the end of each period, ex vivo and in vitro platelet aggregation, and variables of coagulation, fibrinolysis, and hematology were evaluated. In men, ex vivo platelet aggregation time as measured by filtragometry (P = 0.036 for diet effects) was favorably prolonged during consumption of the linoleic acid diet compared with the stearic acid diet (P = 0.040), but there was no difference with consumption of the oleic acid diet (P = 0.198). In vitro platelet aggregation induced by collagen and ADP, and variables of coagulation (factor VII amidolytic activity and concentrations of fibrinogen and prothrombin fragment 1 and 2) and fibrinolysis [plasminogen activator inhibitor (PAI) activity and concentrations of tissue plasminogen activator (tPA)/PAI-1 complexes] did not differ among the 3 diets. The mean platelet volume of the subjects decreased during consumption of the stearic acid diet by 0.32 fL compared with the oleic acid diet (P < 0.001) and by 0.35 fL compared with the linoleic acid diet (P < 0.001). In conclusion, our results do not suggest that stearic acid is highly thrombogenic compared with oleic and linoleic acids.

Adenosine Diphosphate↗

PubMed2005

Metabolic and health effects of isomeric fatty acids.

PURPOSE OF REVIEW: Isomeric fatty acids have the same number of carbon and hydrogen atoms, but may have distinct metabolic and health effects. Two well-known examples of isomeric fatty acids are cis and trans monounsaturated fatty acids, and conjugated isomers of linoleic acid (CLA). The purpose of this review is to summarize recent findings from human studies on the metabolic and health effects of these two classes of isomeric fatty acids. RECENT FINDINGS: Apart from an unfavorable effect on serum lipoproteins, trans monounsaturated fatty acids from hydrogenated oils may increase plasma markers for a low-grade inflammatory state. From epidemiological studies, however, it is not possible to conclude if effects of ruminant and industrial trans fatty acids on cardiovascular risk are different. In contrast to in-vitro and animal studies, there are no indications that in humans the two most common CLA isomers (cis9,trans11-CLA and trans10,cis12-CLA) affect body composition differently. Longer-term supplementation, however, may slightly decrease body fat mass without apparent effects on plasma markers for glucose and lipid metabolism. Other studies have even reported adverse effects of CLA supplementation on insulin resistance and lipid peroxidation. SUMMARY: Evidence is increasing that trans monounsaturated fatty acids from hydrogenated oils increase plasma markers of low-grade chronic inflammation. From epidemiological studies, however, it is not clear if effects of ruminant and industrial trans fatty acids on cardiovascular risk are different. Effects of CLA on body composition remain controversial and more research is needed before the widely available CLA supplements should be advocated as an adjunct to control body weight.

Animals↗