Effect of cheese consumption on blood lipids: a systematic review and meta-analysisi of randomized controlled trials
Goede, J. de; Geleijnse, J.M. ; Ding, E.L. ; Soedamah-Muthu, S.S. - \ 2015
Nutrition Reviews 73 (2015)5. - ISSN 0029-6643 - p. 259 - 275.
coronary-heart-disease - low-density-lipoprotein - fecal fat excretion - cardiovascular-disease - serum-cholesterol - normolipidemic volunteers - clinical-trials - dietary-intake - dairy foods - milk-fat
Context: Cheese may affect lipids and lipoproteins differently than other high-fat dairy foods. Objective: The present systematic review and meta-analysis was performed to evaluate randomized controlled trials that examined the effect of cheese consumption compared with another food product on blood lipids and lipoproteins. Data Sources: A systematic literature search of the MEDLINE, Embase, Scopus, CAB Abstracts, the Cochrane Controlled Trials Register, and the clinicaltrials.gov website was performed. Study Selection: A total of 12 randomized controlled trials (RCTs) were identified that examined the effect of cheese consumption on blood lipids and lipoproteins in healthy adults. Data Extraction: A meta-analysis of 5 RCTs that compared the effects of hard cheese and butter, both of which had a similar ratio of polyunsaturated fatty acids to saturated fatty acids (P/S ratio), was performed. Data Synthesis: Compared with butter intake, cheese intake (weighted mean difference: 145.0 g/d) reduced low-density lipoprotein cholesterol (LDL-C) by 6.5% (-0.22 mmol/l; 95%CI: -0.29 to -0.14) and high-density lipoprotein cholesterol (HDL-C) by 3.9% (-0.05 mmol/l; 95%CI: -0.09 to -0.02) but had no effect on triglycerides. Compared with intake of tofu or fat-modified cheese, cheese intake increased total cholesterol or LDL-C, as was expected on the basis of the P/S ratio of the diets. There was insufficient data to compare intake of cheese with intake of other foods. Conclusion: Despite the similar P/S ratios of hard cheese and butter, consumption of hard cheese lowers LDL-C and HDL-C when compared with consumption of butter. Whether these findings can be attributed to calcium, specific types of saturated fatty acids, or the food matrix of cheese warrants further research.
Molecular mechanisms underlying the potential antiobesity-related diseases effect of cocoa polyphenols
Ali, F. ; Ismail, A. ; Kersten, A.H. - \ 2014
Molecular Nutrition & Food Research 58 (2014)1. - ISSN 1613-4125 - p. 33 - 48.
low-density-lipoprotein - diet-induced obesity - flavanol-rich cocoa - high-fat diet - nf-kappa-b - ldl oxidative susceptibility - alpha-mediated inflammation - insulin-resistance - dark chocolate - in-vitro
Obesity and related metabolic diseases (e.g., type 2 diabetes, cardiovascular diseases, and hypertension) are the most prevailing nutrition-related issues in the world. An emerging feature of obesity is their relationship with chronic inflammation that begins in white adipose tissue and eventually becomes systemic. One potential dietary strategy to reduce glucose intolerance and inflammation is consumption of polyphenol-rich cocoa-like cocoa or their by-products. In vitro as well as in vivo data indicate that cocoa polyphenols (CPs) may exhibit antioxidant and anti-inflammatory properties. Polyphenols commonly found in cocoa have been reported to regulate lipid metabolism via inducing metabolic gene expression or activating transcription factors that regulate the expression of numerous genes, many of which play an important role in energy metabolism. Currently, several molecular targets (e.g., nuclear factor Kappa B, activated protein-1, peroxisome proliferator-activated receptors, liver X receptors, and adiponectin gene) have been identified, which may explain potential beneficial obesity-associated diseases effects of CPs. Further studies have been performed regarding the protective effects of CPs against metabolic diseases by suppressing transcription factors that antagonize lipid accumulation. Thus, polyphenols-rich cocoa products may diminish obesity-mediated metabolic diseases by multiple mechanisms, thereby attenuating chronic inflammation.
Physiological regulation of lipoprotein lipase
Kersten, A.H. - \ 2014
Biochimica et Biophysica Acta. Molecular and Cell Biology of Lipids 1841 (2014)7. - ISSN 1388-1981 - p. 919 - 933.
brown adipose-tissue - low-density-lipoprotein - tumor-necrosis-factor - angiopoietin-like protein - monocyte-derived macrophages - triglyceride-rich lipoproteins - clearing-factor lipase - activated receptor-alpha - human skeletal-muscle - foam cell-formation
The enzyme lipoprotein lipase (LPL), originally identified as the clearing factor lipase, hydrolyzes triglycerides present in the triglyceride-rich lipoproteins VLDL and chylomicrons. LPL is primarily expressed in tissues that oxidize or store fatty acids in large quantities such as the heart, skeletal muscle, brown adipose tissue and white adipose tissue. Upon production by the underlying parenchymal cells, LPL is transported and attached to the capillary endothelium by the protein GPIHBP1. Because LPL is rate limiting for plasma triglyceride clearance and tissue uptake of fatty acids, the activity of LPL is carefully controlled to adjust fatty acid uptake to the requirements of the underlying tissue via multiple mechanisms at the transcriptional and post-translational level. Although various stimuli influence LPL gene transcription, it is now evident that most of the physiological variation in LPL activity, such as during fasting and exercise, appears to be driven via post-translational mechanisms by extracellular proteins. These proteins can be divided into two main groups: the liver-derived apolipoproteins APOC1, APOC2, APOC3, APOA5, and APOE, and the angiopoietin-like proteins ANGPTL3, ANGPTL4 and ANGPTL8, which have a broader expression profile. This review will summarize the available literature on the regulation of LPL activity in various tissues, with an emphasis on the response to diverse physiological stimuli.
Overexpression of angiopoietin-like protein 4 protects against atherosclerosis development
Georgiadi, A. ; Wang, Y. ; Stienstra, R. ; Tjeerdema, N. ; Janssen, A. ; Stalenhoef, A. ; Vliet, A. van der; Roos, J.A. de; Tamsma, J.T. ; Smit, J.W. ; Tan, N.S. ; Müller, M.R. ; Rensen, P.C. ; Kersten, A.H. - \ 2013
Arteriosclerosis Thrombosis and Vascular Biology 33 (2013)7. - ISSN 1079-5642 - p. 1529 - 1537.
low-density-lipoprotein - mouse peritoneal-macrophages - foam cell-formation - transgenic mice - lipase - angptl4 - expression - gene - hyperlipoproteinemia - hyperlipidemia
Objective—Macrophage foam cells play a crucial role in several pathologies including multiple sclerosis, glomerulosclerosis, and atherosclerosis. Angiopoietin-like protein 4 (Angptl4) was previously shown to inhibit chyle-induced foam cell formation in mesenteric lymph nodes. Here we characterized the regulation of Angptl4 expression in macrophages and examined the impact of Angptl4 on atherosclerosis development. Approach and Results—Macrophage activation elicited by pathogen-recognition receptor agonists decreased Angptl4 expression, whereas lipid loading by intralipid and oxidized low-density lipoprotein increased Angptl4 expression. Consistent with an antilipotoxic role of Angptl4, recombinant Angptl4 significantly decreased uptake of oxidized low-density lipoprotein by macrophages, via lipolysis-dependent and -independent mechanisms. Angptl4 protein was detectable in human atherosclerotic lesions and localized to macrophages. Transgenic overexpression of Angptl4 in atherosclerosis-prone apolipoprotein E*3-Leiden mice did not significantly alter plasma cholesterol and triglyceride levels. Nevertheless, Angptl4 overexpression reduced lesion area by 34% (P
A state-of-the-art overview of the effect of metabolic conjugation on the biological activity of flavonoids
Beekmann, K. ; Actis-Goretta, L. ; Bladeren, P.J. van; Dionisi, F. ; Destaillats, F. ; Rietjens, I. - \ 2012
Food & Function 3 (2012)10. - ISSN 2042-6496 - p. 1008 - 1018.
low-density-lipoprotein - in-vivo metabolites - tea polyphenol (-)-epigallocatechin-3-gallate - organic anion transporters - induced cell-death - quercetin glucuronides - antioxidant properties - cardiovascular-disease - adhesion molecules - plasma metabolites
Diets rich in flavonoids are associated with various positive health effects. Most in vitro research conducted to elucidate the modes of action of flavonoids uses flavonoid aglycones, but not their circulating conjugated metabolites. Conjugation alters the physico-chemical properties of flavonoids and it is widely assumed that this can affect their biological activity. This article gives a state-of-the-art overview of scientific literature reporting on the effect of metabolic conjugation on the biological activity of flavonoids. The biological activity of flavonoid aglycones is compared to that of their conjugates for a broad range of endpoints. Even though there is only limited literature available, it is shown that contrary to common belief, conjugation does not always decrease the biological activity of flavonoids. There are also endpoints which are unaffected by conjugation, and endpoints on which the conjugates have a higher or inverse activity when compared to the aglycone. The effects of conjugation can differ depending on the type and position of conjugation, the flavonoid concentration, the endpoint studied and the assay system used so that no general rules can be deducted. It is concluded that further studies on the effects of conjugation have to be done on a case-by-case basis, and characterization of the stability and metabolic fate of the flavonoids in the assay system under consideration is needed to avoid false positive or false negative outcomes.
Low Serum Glutathione Peroxidase Activity Is Associated with Increased Cardiovascular Mortality in Individuals with Low HDLc’s
Buijsse, B. ; Lee, D.H. ; Steffen, L. ; Erickson, R.R. ; Luepker, R.V. ; Jacobs, D.R. ; Holtzman, J.L. - \ 2012
PLoS ONE 7 (2012)6. - ISSN 1932-6203
minnesota-heart-survey - low-density-lipoprotein - human-plasma - lipid peroxides - risk-factors - disease - cholesterol - trends - atherosclerosis - purification
Background Since oxidized LDL is thought to initiate atherosclerosis and the serum glutathione peroxidase (GPx3) reduces oxidized lipids, we investigated whether high GPx3 activity reduces cardiovascular disease (CVD) mortality. Methods We determined GPx3 in stored samples from the Minnesota Heart Survey of 130 participants who after 5 to 12 years of follow-up had died of CVD and 240 controls. Participants were 26 to 85 years old and predominantly white. In a nested case-control, study we performed logistic regressions to calculate odds ratios (OR) adjusted for age, sex, baseline year, body mass index, smoking, alcohol intake, physical activity, total and HDL cholesterols, systolic blood pressure, serum glucose and gamma glutamyltransferase (GTT) activity. The referent was the quartile with the highest GPx3 activity (quartile 4). Results OR’s for CVD mortality for increasing quartiles of GPx3 were 2.37, 2.14, 1.83 and 1.00 (P for trend 0.02). This inverse correlation was confined to those with HDLc’s below the median (P for interaction, 0.006). The OR’s for increasing quartiles of GPx3 in this group were 6.08, 5.00, 3.64 and 1.00 (P for trend, 0.002). Conclusions Individuals with both low HDLc and GPx3 activity are at markedly increased risk for death from CVD.
Antioxidative properties of flavonoids
Bowedes, T.C.F. ; Luttikhold, J. ; Stijn, M.F.M. van; Visser, M. ; Norren, K. van; Vermeulen, M.A.R. ; Leeuwen, P.A.M. - \ 2011
Current Organic Chemistry 15 (2011)15. - ISSN 1385-2728 - p. 2616 - 2626.
spontaneously hypertensive-rats - myocardial ischemia-reperfusion - low-density-lipoprotein - nf-kappa-b - prevents endothelial dysfunction - reduces blood-pressure - coronary heart-disease - green tea polyphenol - dietary polyphenols - in-vivo
Evidence accumulates that a family of plant compounds, known as flavonoids, can prevent or slow down the progression of cardiovascular diseases, cancer, inflammatory and neurodegenerative diseases. Flavonoids are considered beneficial, this is often attributed to their powerful antioxidant properties. In this role, certain types of flavonoids are considered to be far more powerful than the two most common antioxidants, vitamin C and vitamin E, at preventing cellular damage brought on by free radicals. Interestingly, flavonoids exert those activities not only through direct radical scavenging, but also through regulating nitric oxide, and chelating metals. In addition, flavonoids are thought to facilitate/promote other important biological processes, resulting in modulation of enzymes, a decrease in leukocyte immobilization, inhibition of cell proliferation and angiogenesis, and effects on signaling pathways. The results of in vitro studies have demonstrated that the antioxidative property of flavonoids is unambiguous; however it is still not supported by strong consistent evidence in vivo. Therefore, the antioxidant theory as a mechanism of action of flavonoids is controversial. As a result, flavonoids are hypothesized to exert their activities partly through cell signaling pathways. This review intends to acquaint the reader with different pathways in which flavonoids function or might function. Furthermore, we will provide insight into the beneficial health effects of these substances
The Biological Relevance of Direct Antioxidant Effects of Polyphenols for Cardiovascular Health in Humans Is Not Established
Hollman, P.C.H. ; Cassidy, A. ; Comte, B. ; Heinonen, M. ; Richelle, M. ; Richling, E. ; Serafini, M. ; Scalbert, A. ; Sies, H. ; Vidry, S. - \ 2011
The Journal of Nutrition 141 (2011)5. - ISSN 0022-3166 - p. 989S - 1009S.
performance liquid-chromatography - coronary-heart-disease - lipid-peroxidation products - low-density-lipoprotein - black tea consumption - flavanol-rich cocoa - serum uric-acid - oxidative stress status - grape seed extract - major food sources
Human studies provide evidence for beneficial effects of polyphenol-rich foods on cardiovascular health. The antioxidant activity of polyphenols potentially explains these effects, but is the antioxidant activity a reliable predictor for these effects? An International Life Sciences Institute Europe working group addressed this question and explored the potential of antioxidant claims for polyphenols in relation to cardiovascular health by using the so-called Process for the Assessment of Scientific Support for Claims on Foods project criteria. In this process, analytical aspects of polyphenols, their occurrence in foods, dietary intake, and bioavailability were reviewed. Human studies on polyphenols and cardiovascular health were reviewed together with methods for biomarkers of oxidative damage and total antioxidant capacity (TAC). In retrospective studies, F2-isoprostanes and oxidized LDL, the most reliable biomarkers of lipid peroxidation, and measures for TAC showed the expected differences between cardiovascular disease patients and healthy controls, but prospective studies are lacking, and a causal relationship between these biomarkers and cardiovascular health could not be established. Therefore, the physiological relevance of a potential change in these biomarkers is unclear. We found limited evidence that some types of polyphenol-rich products modify these biomarkers in humans. A direct antioxidant effect of polyphenols in vivo is questionable, however, because concentrations in blood are low compared with other antioxidants and extensive metabolism following ingestion lowers their antioxidant activity. Therefore, the biological relevance of direct antioxidant effects of polyphenols for cardiovascular health could not be established. Overall, although some polyphenol-rich foods exert beneficial effects on some biomarkers of cardiovascular health, there is no evidence that this is caused by improvements in antioxidant function biomarkers (oxidative damage or antioxidant capacity). J. Nutr. 141: 989S-1009S, 2011.
A Role of the Bile Salt Receptor FXR in Atherosclerosis
Hageman, J. ; Herrema, H.J. ; Groen, A.K. ; Kuipers, F. - \ 2010
Arteriosclerosis Thrombosis and Vascular Biology 30 (2010)8. - ISSN 1079-5642 - p. 1519 - 1528.
farnesoid-x-receptor - low-density-lipoprotein - vascular smooth-muscle - reverse cholesterol transport - small heterodimer partner - apolipoprotein-a-i - nuclear receptor - deficient mice - acid synthesis - targeted disruption
This study reviews current insights into the role of bile salts and bile salt receptors on the progression and regression of atherosclerosis. Bile salts have emerged as important modifiers of lipid and energy metabolism. At the molecular level, bile salts regulate lipid and energy homeostasis mainly via the bile salt receptors FXR and TGR5. Activation of FXR has been shown to improve plasma lipid profiles, whereas Fxr(-/-) mice have increased plasma triglyceride and very-low-density lipoprotein levels. Nevertheless, high-density lipoprotein cholesterol levels are increased in these mice, suggesting that FXR has both anti-and proatherosclerotic properties. Interestingly, there is increasing evidence for a role of FXR in "nonclassical" bile salt target tissues, eg, vasculature and macrophages. In these tissues, FXR has been shown to influence vascular tension and regulate the unloading of cholesterol from foam cells, respectively. Recent publications have provided insight into the antiinflammatory properties of FXR in atherosclerosis. Bile salt signaling via TGR5 might regulate energy homeostasis, which could serve as an attractive target to increase energy expenditure and weight loss. Interventions aiming to increase cholesterol turnover (eg, by bile salt sequestration) significantly improve plasma lipid profiles and diminish atherosclerosis in animal models. Bile salt metabolism and bile salt signaling pathways represent attractive therapeutic targets for the treatment of atherosclerosis
Feeding conditions control the expression of genes involved in sterol metabolism in peripheral blood mononuclear cells of normoweight and diet-induced (cafeteria) obese rats
Caimari, A. ; Oliver, P. ; Rodenburg, W. ; Keijer, J. ; Palou, A. - \ 2010
Journal of Nutritional Biochemistry 21 (2010)11. - ISSN 0955-2863 - p. 1127 - 1133.
low-density-lipoprotein - acute regulatory protein - coa-cholesterol acyltransferase - beta-methylglutaryl-coenzyme - messenger-rna expression - signal-transduction - human-lymphocytes - lipid-synthesis - adipose-tissue - in-vivo
Peripheral blood mononuclear cells (PBMC) are easily obtainable cells from blood whose gene expression profiles have been proven to be highly robust in distinguishing a disease state from healthy state. Sterol metabolism is of physiological importance, and although its nutritional response in liver has been described, it is poorly studied in PBMC. To examine if PBMC sterol metabolism reflects diet-induced physiological responses, we analysed the whole genome gene expression response of PBMC and focused on sterol metabolism-related genes affected by different feeding conditions (ad libitum feeding, fasting, and refeeding) in normoweight (control) rats and in diet-induced (cafeteria) obese rats. Our results of microarray analysis show that, in control rats, 21 genes involved in sterol metabolism were regulated by the different feeding conditions, whereas in cafeteria-obese rats, only seven genes showed a changed expression. Most of the genes identified were classified into three pathways: sterol biosynthesis, cholesterol transport and uptake and sterol signaling. The expression profile of these genes was similar to that previously described for liver, decreasing in response to fasting conditions and recovering the levels found in fed animals after 6-h-refeeding. In addition, our data and the comparable expression pattern of sterol metabolism-related genes between PBMC and liver suggest similar sterol regulatory element-binding protein-mediated regulatory mechanisms in response to feeding conditions in both tissues. In conclusion, the expression of genes involved in sterol metabolism is highly controlled by feeding conditions in PBMC of control rats, but this control is impaired in cafeteria-obese animals. The pathophysiological significance of this impairment requires further investigation.
Triglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies
Kromhout, D. - \ 2010
The Lancet 375 (2010)9726. - ISSN 0140-6736 - p. 1634 - 1639.
low-density-lipoprotein - apolipoprotein-a-v - transfer protein - heart-disease - myocardial-infarction - metabolic syndrome - rich lipoproteins - risk - dyslipidemia - association
Background -Whether triglyceride-mediated pathways are causally relevant to coronary heart disease is uncertain. We studied a genetic variant that regulates triglyceride concentration to help judge likelihood of causality. Methods - We assessed the -1131T>C (rs662799) promoter polymorphism of the apolipoprotein A5 (APOA5) gene in relation to triglyceride concentration, several other risk factors, and risk of coronary heart disease. We compared disease risk for genetically-raised triglyceride concentration (20 842 patients with coronary heart disease, 35 206 controls) with that recorded for equivalent differences in circulating triglyceride concentration in prospective studies (302 430 participants with no history of cardiovascular disease; 12 785 incident cases of coronary heart disease during 2·79 million person-years at risk). We analysed -1131T>C in 1795 people without a history of cardiovascular disease who had information about lipoprotein concentration and diameter obtained by nuclear magnetic resonance spectroscopy. Findings - The minor allele frequency of -1131T>C was 8% (95% CI 7-9). -1131T>C was not significantly associated with several non-lipid risk factors or LDL cholesterol, and it was modestly associated with lower HDL cholesterol (mean difference per C allele 3·5% [95% CI 2·6-4·6]; 0·053 mmol/L [0·039-0·068]), lower apolipoprotein AI (1·3% [0·3-2·3]; 0·023 g/L [0·005-0·041]), and higher apolipoprotein B (3·2% [1·3-5·1]; 0·027 g/L [0·011-0·043]). By contrast, for every C allele inherited, mean triglyceride concentration was 16·0% (95% CI 12·9-18·7), or 0·25 mmol/L (0·20-0·29), higher (p=4·4×10-24). The odds ratio for coronary heart disease was 1·18 (95% CI 1·11-1·26; p=2·6×10-7) per C allele, which was concordant with the hazard ratio of 1·10 (95% CI 1·08-1·12) per 16% higher triglyceride concentration recorded in prospective studies. -1131T>C was significantly associated with higher VLDL particle concentration (mean difference per C allele 12·2 nmol/L [95% CI 7·7-16·7]; p=9·3×10-8) and smaller HDL particle size (0·14 nm [0·08-0·20]; p=7·0×10-5), factors that could mediate the effects of triglyceride. Interpretation - These data are consistent with a causal association between triglyceride-mediated pathways and coronary heart disease. Funding - British Heart Foundation, UK Medical Research Council, Novartis
Fortification of lysine for improving protein quality in multiple-fortified quick cooking rice : Review
Wongmetinee, T. ; Boonstra, A. ; Zimmermann, M.B. ; Chavasit, V. - \ 2009
European Journal of Clinical Nutrition 63 (2009)S3. - ISSN 0954-3007 - p. S21 - S21.
coronary-heart-disease - conjugated linoleic-acid - type-2 diabetes-mellitus - hydrogenated soybean oil - low-density-lipoprotein - c-reactive protein - sudden cardiac death - fed controlled diets - adipose body tissue - insulin sensitivity
Previous studies in Thailand indicated that rice-based complementary foods of breast-fed infants normally provided inadequate iron and calcium. Quick-cooking rice fortified with different nutrients was therefore developed. The idea of lysine fortification was based on the fact that lysine is a limiting amino acid in rice. The objective of this study was to determine the feasibility of producing quick-cooking rice (MFQCR) fortified with adequate levels of vitamins, minerals and lysine together with an assessment of lysine intake among Thai infants. Lysine together with iron, calcium, zinc, thiamin and folate was fortified into broken rice to meet the requirements for infants aged 6-24 mo. Lysine loss and changes in physical and sensory qualities were determined during a shelf-life study under accelerated condition. To assess the lysine intake among infants, 24 hour-recall data from Thai National Food Consumption Survey (2006) among infants aged 6-24 mo in Central Thailand was used. It was considered feasible to produce lysine-fortified MFQCR, and using it did not affect the intake of infants. The lysine requirement was most fulfilled in infant aged 12-24 mo being fed with 3 meals. Food consumption data showed that the daily lysine intake was certainly adequate, and no difference between infants from low- and highincome households was found. Lysine fortification in MFQCR might not be beneficial to infants in Central Thailand; however, it is still considered more required in countries where the populations consume cereal-based diet, and have no access to good quality protein e.g. Cambodia, Indonesia and North Korea
Efficient isolation of major procyanidin A-type dimers from peanut skins and B-type dimers from grape seeds
Appeldoorn, M.M. ; Sanders, M.B. ; Vincken, J.P. ; Cheynier, V. ; Guerneve, C. Le; Gruppen, H. - \ 2009
Food Chemistry 117 (2009)4. - ISSN 0308-8146 - p. 713 - 720.
performance liquid-chromatography - low-density-lipoprotein - reversed-phase hplc - antioxidant activity - proanthocyanidins - cocoa - polymerization - fractionation - separation - extract
In order to fully explore the biofunctional potential of proanthocyanidins (PA), isolated and well-characterised PA dimers are of great importance. Current methods to obtain pure A- and B-type dimers are laborious, because they comprise multiple chromatographic steps, often yielding only one or two specific dimers. In the current study, an efficient isolation procedure is described, to isolate a large variety of A-type dimers from peanut skins and B-type dimers from grape seeds. Yields increased 20-400 times for A-type dimers and about 10 times for B-type dimers compared to other methods with a lesser number of chromatographic steps. Dimers isolated from peanut skins were identified as; epicatechin-(2-O-7, 4-8)-catechin (A1), epicatechin-(2-O-7, 4-8)-epicatechin (A2), epicatechin-(2-O-7, 4-6)-catechin, epicatechin-(2-O-7, 4-8)-entcatechin, isolated from peanut skins for the first time, and epicatechin-(4-6)-catechin (B7). Dimers from grape seeds were identified as; epicatechin-(4-8)-catechin (B1), epicatechin-(4-8)-epicatechin (B2), catechin-(4-8)-catechin (B3) and catechin-(4-8)-epicatechin (B4)
Dietary determinants of subclinical inflammation, dyslipidemia and components of the metabolic syndrome in overweight children: a review
Zimmermann, M.B. ; Aeberli, I. - \ 2008
International Journal of Obesity 32 (2008). - ISSN 0307-0565 - p. S11 - S18.
c-reactive protein - retinol-binding-protein - tumor-necrosis-factor - cardiovascular risk-factors - insulin-resistance syndrome - low-density-lipoprotein - vitamin-a-deficiency - grade systemic inflammation - increased oxidative stress - unsaturated fatty-acids
Objective: To review and summarize the dietary determinants of the metabolic syndrome, subclinical inflammation and dyslipidemia in overweight children. Design: Review of the current literature, focusing on pediatric studies. Participants: Normal weight, overweight, or obese children and adolescents. Results: There is a growing literature on the metabolic effects of excess body fat during childhood. However, few pediatric studies have examined the dietary determinants of obesity-related metabolic disturbances. From the available data, it appears that dietary factors are not only important environmental determinants of adiposity, but also may affect components of the metabolic syndrome and modulate the actions of adipokines. Dietary total fat and saturated fat are associated with insulin resistance and high blood pressure, as well as obesity-related inflammation. In contrast to studies in adults, resistin and adiponectin do not appear to be closely linked to insulin resistance or dyslipidemia in childhood. However, circulating leptin and retinol-binding protein (RBP) 4 correlate well with obesity, central obesity and the metabolic syndrome in children. Intakes of antioxidant vitamins tend to be low in obese children and may be predictors of subclinical inflammation. Higher fructose intake from sweets and sweetened drinks in overweight children has been linked to decreased low-density lipoprotein (LDL) particle size. Conclusions: Dietary interventions aimed at reducing intakes of total fat, saturated fat and free fructose, whereas increasing antioxidant vitamin intake may be beneficial in overweight children. More research on the relationships between dietary factors and the metabolic changes of pediatric obesity may help to identify the dietary changes to reduce health risks.
Clinical Care and Delivery: Paraoxonase 1 phenotype distribution and activity differs in subjects with newly diagnosed Type 2 diabetes (the CODAM Study)
Berg, S.W. van den; Jansen, E.H.J. ; Kruijshoop, M. ; Beekhof, P.K. ; Blaak, E.E. ; Kallen, C.J.H. van der; Greevenbroek, M.M.J. van; Feskens, E.J.M. - \ 2008
Diabetic medicine 25 (2008)2. - ISSN 0742-3071 - p. 186 - 193.
low-density-lipoprotein - impaired glucose-tolerance - coronary-heart-disease - islet beta-cells - serum paraoxonase - oxidative stress - insulin-resistance - gene polymorphism - iron stores - follow-up
Aims Paraoxonase 1 (PON1) is an antioxidant high-density lipoprotein-bound enzyme, which was recently found to be expressed in the islets of Langerhans. A substitution (Q/R) at position 192 results in enzymes with different activity. Oxidation has been implicated in the onset of diabetes, and it can be hypothesized that PON1 may have a protective effect on diabetes. Our aim was to compare PON1 activities and PON1 Q/R phenotypes in subjects with different degrees of glucose intolerance. Methods We examined 566 members of the Cohort study of Diabetes and Atherosclerosis Maastricht (CoDAM), including subjects with normal glucose tolerance (NGT, n = 298), impaired glucose regulation (IGR, n = 128), newly diagnosed Type 2 diabetes (nDM, n = 78) and treated, that is to say known, Type 2 diabetes (kDM, n = 64). PON1 activity was measured in serum using paraoxon and diazoxon as substrates. The PON1 phenotype was determined using two-dimensional enzyme analysis. Results The RR-phenotype was significantly more frequent in nDM compared with NGT subjects (14.1 vs. 6.0%, P = 0.05). Adjusted for the PON1 phenotype, subjects with nDM had significant lower PON1 activity towards paraoxon and diazoxon than subjects with NGT. Adjusted odds ratios comparing the RR-variant with the QQ-variant were 2.17 [95% confidence interval (CI): 0.90¿5.24] for impaired glucose tolerance, 2.84 (95% CI: 1.03¿7.83) for nDM, 2.13 (95% CI; 0.61¿7.42) for kDM and 2.65 (95% CI: 1.10¿6.40) for total diabetes mellitus. Conclusions An aberrant PON1 phenotype distribution and PON1 activity were observed in early diabetes. In addition, the higher state of oxidative stress may affect the future development of complications.
High folic acid increases cell turnover and lowers differentiation and iron content in human HT29 colon cancer cells
Pellis, E.P.M. ; Dommels, Y.E.M. ; Venema, D.P. ; Polanen, A. van; Lips, E. ; Baykus, H. ; Kok, F.J. ; Kampman, E. ; Keijer, J. - \ 2008
The British journal of nutrition 99 (2008)4. - ISSN 0007-1145 - p. 703 - 708.
low-density-lipoprotein - folate-deficiency - colorectal-cancer - gene-expression - dna methylation - mismatch repair - dietary-folate - apoptosis - disease - risk
Folate, a water-soluble B vitamin, is a cofactor in one-carbon metabolism and is essential for DNA synthesis, amino acid interconversion, methylation and, consequently, normal cell growth. In animals with existing pre-neoplastic and neoplastic lesions, folic acid supplementation increases the tumour burden. To identify processes that are affected by increased folic acid levels, we compared HT29 human colon cancer cells exposed to a chronic supplemental (100 ng/ml) level of folic acid to cells exposed to a normal (10 ng/ml) level of folic acid, in the presence of vitamin B12 and other micronutrients involved in the folate¿methionine cycle. In addition to higher intracellular folate levels, HT29 cells at 100 ng folic acid/ml displayed faster growth and higher metabolic activity. cDNA microarray analysis indicated an effect on cell turnover and Fe metabolism. We fully confirmed these effects at the physiological level. At 100 ng/ml, cell assays showed higher proliferation and apoptosis, while gene expression analysis and a lower E-cadherin protein expression indicated decreased differentiation. These results are in agreement with the promoting effect of folic acid supplementation on established colorectal neoplasms. The lower expression of genes related to Fe metabolism at 100 ng folic acid/ml was confirmed by lower intracellular Fe levels in the cells exposed to folic acid at 100 ng/ml. This suggests an effect of folate on Fe metabolism
Both alpha- and ß-Carotene, but Not Tocopherols and Vitamin C, are Inversely Related to 15-Year Cardiovascular Mortality in Dutch Elderly Men 1,2
Buijsse, B. ; Feskens, E.J.M. ; Kwape, L. ; Kok, F.J. ; Kromhout, D. - \ 2008
The Journal of Nutrition 138 (2008)2. - ISSN 0022-3166 - p. 344 - 350.
coronary-heart-disease - acute myocardial-infarction - low-density-lipoprotein - antioxidant vitamins - combined supplementation - endothelial dysfunction - oxidation resistance - dietary antioxidants - lipid-peroxidation - randomized-trials
The role of ß-carotene, -tocopherol, and vitamin C in the prevention of cardiovascular diseases (CVD) is controversial. Prospective studies on -tocopherol and carotenoids other than ß-carotene are sparse. We assessed relations between the intake of different carotenoids, - and -tocopherol, and vitamin C with 15-y CVD mortality in elderly men who participated in the Zutphen Elderly Study. Information on diet and potential confounding factors was collected in 1985, 1990, and 1995. In 1985, 559 men (mean age 72 y) free of chronic diseases were included in the current analysis. After 15 y of follow-up, comprising 5744 person-years, 197 men had died from CVD. After adjustment for age, smoking, and other potential lifestyle and dietary confounders, relative risks (RR) (95% CI) of CVD death for a 1-SD increase in intake were 0.81 (0.66¿0.99) for -carotene and 0.80 (0.66¿0.97) for ß-carotene. Carrots were the primary source of - and ß-carotene and their consumption was related to a lower risk of death from CVD (adjusted RR, 0.83; 95% CI = 0.68¿1.00). Intakes of carotenoids other than - and ß-carotene were not associated with CVD mortality, nor were vitamin C and - and tocopherol. In conclusion, dietary intakes of -carotene and ß-carotene are inversely associated with CVD mortality in elderly men. This study does not indicate an important role for other carotenoids, tocopherols, or vitamin C in lowering the risk of CVD death.
PPAR - and dyslipidemia
Duval, C.N.C. ; Müller, M.R. ; Kersten, A.H. - \ 2007
Biochimica et Biophysica Acta. Molecular and Cell Biology of Lipids 1771 (2007)8. - ISSN 1388-1981 - p. 961 - 971.
proliferator-activated-receptor - coronary-artery-disease - low-density-lipoprotein - apolipoprotein-c-iii - rev-erb-alpha - diabetes atherosclerosis intervention - reverse cholesterol transport - angiopoietin-like protein-4 - chylomicron-like emulsions - coenzyme
Dyslipidemia is defined by abnormal levels of plasma lipoproteins. Several different types of dyslipidemia can be distinguished. An important group of drugs used in the treatment of dyslipidemia are the fibrates. Fibrates serve as agonists for the peroxisome proliferator-activated receptor alpha (PPAR¿), a ligand-activated transcription factor that belongs to the superfamily of nuclear hormone receptors. By binding to response elements mostly present in the promoter of target genes, PPAR¿ governs the expression of numerous genes involved in a variety of metabolic processes. Activation of PPAR¿ results in a reduction of plasma TG levels, which is achieved by: (1) induction of genes that decrease the availability of TG for hepatic VLDL secretion, and (2) induction of genes that promote lipoprotein lipase-mediated lipolysis of TG-rich plasma lipoproteins. The stimulatory effect of PPAR¿ on plasma HDL levels in humans, which is opposite to what is observed in mice, appears to be mainly mediated via increased production of APOA1 and APOA2, the apolipoprotein constituents of HDL. Apart from its major actions outlined above, PPAR¿ modulates lipoprotein metabolism in several other ways, mostly via direct up-regulation of specific PPAR¿ target genes. By taking into account novel insights into the metabolism of plasma lipoproteins and by considering the latest information on PPAR¿-dependent gene regulation, a fresh perspective on the molecular mechanisms underlying the plasma lipoprotein modulating effect of PPAR¿ is presented.
Proteome analysis suggests that mitochondrial dysfunction in stressed endothelial cells is reversed by a soy extract and isolated isoflavones
Fuchs, D. ; Dirscherl, B. ; Schroot, J.H. ; Daniel, H. ; Wenzel, U. - \ 2007
Journal of Proteome Research 6 (2007)6. - ISSN 1535-3893 - p. 2132 - 2142.
low-density-lipoprotein - smooth-muscle cells - oxidized-ldl - platelet-aggregation - hyperglycemic damage - phyto-estrogens - genistein - pathways - superoxide - expression
Apoptosis is a driving force in atherosclerosis development. A soy extract or a combination of the soy isoflavones genistein and daidzein inhibited apoptosis induced by oxidized LDL in endothelial cells. Proteome analysis revealed that the LDL-induced alterations of numerous proteins were reversed by the extract and the genistein/daidzein mixture but only three protein entities, all functionally linked to mitochondrial dysfunction, were regulated in common by both treatments.
Flavonoids and heart health: Proceedings of the ILSI North America Flavonoids Workshop may 31-june 1, 2005, Washington DC
Erdman, J.W. ; Balentine, D. ; Arab, L. ; Beecher, G. ; Dwyer, J.T. ; Folts, J. ; Harnly, J. ; Hollman, P.C.H. ; Keen, C.L. ; Mazza, G. ; Messina, M. ; Scalbert, A. ; Vita, J. ; Williamson, G. ; Burrows, J. - \ 2007
The Journal of Nutrition 137 (2007)3. - ISSN 0022-3166 - p. 718s - 737s.
low-density-lipoprotein - coronary-artery-disease - potentially anticarcinogenic flavonoids - environmental estrogenic compounds - estradiol-induced tumorigenesis - improves endothelial function - liquid-chromatographic method - catechol o-methyltransferase - ran
This article provides an overview of current research on flavonoids as presented during a workshop entitled, "Flavonoids and Heart Health," held by the ILSI North America Project Committee on Flavonoids in Washington, DC, May 31 and June 1, 2005. Because a thorough knowledge and understanding about the science of flavonoids and their effects on health will aid in establishing dietary recommendations for bioactive components such as flavonoids, a systematic review of the science of select flavonoid classes (i.e., flavonols, flavones, flavanones, isoflavones, flavan-3-ols, anthocyanins, and proanthocyanidins) was presented. The objectives of the workshop were to 1) present and discuss current research on flavonoid intake and the relation between flavonoids and heart health; 2) develop information that could lead to expert consensus on the state-of-the-science of dietary intake of flavonoids on heart health; and 3) summarize and prioritize the research needed to establish the relations between specific flavonoids and heart health. Presentations included the basics of the biology of flavonoids, including the types and distribution in foods, analytical methodologies used to determine the amounts in foods, the bioavailability, the consumption patterns and potential biomarkers of intake, risk assessment and safety evaluation, structure/function claims, and the proposed mechanism(s) of the relation between certain flavonoids and heart health endpoints. Data presented support the concept that certain flavonoids in the diet can be associated with significant health benefits, including heart health. Research gaps were identified to help advance the science.