Nutrition And Toxicology Research Institute Maastricht

Maastricht, Netherlands

Nutrition And Toxicology Research Institute Maastricht

Maastricht, Netherlands
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Van Den Berg E.,Top Institute Food and Nutrition | Van Den Berg E.,University of Groningen | Hospers F.A.P.,University of Groningen | Navis G.,Top Institute Food and Nutrition | And 12 more authors.
Journal of Nephrology | Year: 2011

Diabetic nephropathy is now the most common cause of end-stage renal failure in many countries of the world. Despite increasing implementation of preventive treatment, the chance that an individual diabetic patient will reach end-stage renal failure has been increasing rather than decreasing during recent decades. Current dietary habits in The Netherlands and the rest of the Western world are slowly shifting from relatively alkalinizing (e.g., potatoes and vegetables) toward more acidifying (e.g., rice and meat). Moreover, immigrants who consumed traditional diets in their homelands, usually adapt to Western dietary habits. This phenomenon of diet acculturation could, for instance, be involved in the up to 40 times higher chance of development of end-stage renal failure in association with diabetes in South-Asian immigrants compared with whites, in Western countries. High ingestion of nonvolatile acids with food increases susceptibility for progression to end-stage renal failure. These high dietary acid loads lead to compensatory increases in renal acid excretion and ammoniagenesis. The price paid for maintenance of acid-base homeostasis is renal tubulointerstitial injury, with subsequent decline in renal function and induction of hypertension. The tendency for metabolic acidosis that results from the changing dietary habits could be corrected by a shift toward more alkalinizing food. We hypothesize that promoting such a shift can prevent the epidemic of end-stage renal failure in diabetes. © 2011 Società Italiana di Nefrologia.


Garcia-Rios A.,University of Cordoba, Spain | Perez-Martinez P.,University of Cordoba, Spain | Delgado-Lista J.,University of Cordoba, Spain | Phillips C.M.,University College Dublin | And 15 more authors.
Journal of Nutrition | Year: 2012

Genetic variants of Period 2 (PER2), a circadian clock gene, have been linked to metabolic syndrome (MetS). However, it is still unknown whether these genetic variants interact with the various types of plasma fatty acids. This study investigated whether common single nucleotide polymorphisms (SNPs) in the PER2 locus (rs934945 and rs2304672) interact with various classes of plasma fatty acids to modulate plasma lipid metabolism in 381 participants with MetS in the European LIPGENE study. Interestingly, the rs2304672 SNP interactedwith plasma total SFA concentrations to affect fasting plasma TG, TG-rich lipoprotein (TRL-TG), total cholesterol, apoC-II, apoB, and apoB-48 concentrations (P-interaction< 0.001-0.046). Carriers of the minor allele (GC+GG) with the highest SFA concentration (>median) had a higher plasma TG concentration (P = 0.001) and higher TRL-TG (P< 0.001) than the CC genotype. In addition, participants carrying the minor G allele for rs2304672 SNP and with a higher SFA concentration (>median) had higher plasma concentrations of apo C-II (P<0.001), apo C-III (P=0.009), and apoB-48 (P=0.028) compared with the homozygotes for the major allele (CC). In summary, the rs2304672 polymorphism in the PER2 gene locus may influence lipid metabolism by interacting with the plasma total SFA concentration in participants with MetS. The understanding of these gene-nutrient interactions could help to provide a better knowledge of the pathogenesis in MetS. © 2012 American Society for Nutrition.


Tierney A.C.,University College Dublin | McMonagle J.,University College Dublin | Shaw D.I.,University of Reading | Gulseth H.L.,University of Oslo | And 15 more authors.
International Journal of Obesity | Year: 2011

Background:Excessive energy intake and obesity lead to the metabolic syndrome (MetS). Dietary saturated fatty acids (SFAs) may be particularly detrimental on insulin sensitivity (SI) and on other components of the MetS.Objective:This study determined the relative efficacy of reducing dietary SFA, by isoenergetic alteration of the quality and quantity of dietary fat, on risk factors associated with MetS.Design:A free-living, single-blinded dietary intervention study.Subjects and Methods:MetS subjects (n417) from eight European countries completed the randomized dietary intervention study with four isoenergetic diets distinct in fat quantity and quality: high-SFA; high-monounsaturated fatty acids and two low-fat, high-complex carbohydrate (LFHCC) diets, supplemented with long chain n-3 polyunsaturated fatty acids (LC n-3 PUFAs) (1.2 g per day) or placebo for 12 weeks. SI estimated from an intravenous glucose tolerance test (IVGTT) was the primary outcome measure. Lipid and inflammatory markers associated with MetS were also determined.Results:In weight-stable subjects, reducing dietary SFA intake had no effect on SI, total and low-density lipoprotein cholesterol concentration, inflammation or blood pressure in the entire cohort. The LFHCC n-3 PUFA diet reduced plasma triacylglycerol (TAG) and non-esterified fatty acid concentrations (P0.01), particularly in men.Conclusion:There was no effect of reducing SFA on SI in weight-stable obese MetS subjects. LC n-3 PUFA supplementation, in association with a low-fat diet, improved TAG-related MetS risk profiles. © 2011 Macmillan Publishers Limited All rights reserved.


Phillips C.M.,University College Dublin | Goumidi L.,French Institute of Health and Medical Research | Bertrais S.,University of Paris 13 | Field M.R.,Hitachi Dublin Laboratory | And 15 more authors.
Journal of Lipid Research | Year: 2010

Long-chain acyl CoA synthetase 1 (ACSL1) plays an important role in fatty acid metabolism and triacylglycerol (TAG) synthesis. Disturbance of these pathways may result in dyslipidemia and insulin resistance, hallmarks of the metabolic syndrome (MetS). Dietary fat is a key environmental factor that may interact with genetic determinants of lipid metabolism to affect MetS risk. We investigated the relationship between ACSL1 polymorphisms (rs4862417, rs6552828, rs13120078, rs9997745, and rs12503643) and MetS risk and determined potential interactions with dietary fat in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1,754). GG homozygotes for rs9997745 had increased MetS risk {odds ratio (OR) 1.90 [confidence interval (CI) 1.15, 3.13] ; P = 0.01}, displayed elevated fasting glucose (P = 0.001) and insulin concentrations (P = 0.002) and increased insulin resistance (P = 0.03) relative to the A allele carriers. MetS risk was modulated by dietary fat, whereby the risk conferred by GG homozygosity was abolished among individuals consuming either a low-fat (<35% energy) or a high-PUFA diet (>5.5% energy).jlr In conclusion, ACSL1 rs9997745 influences MetS risk, most likely via disturbances in fatty acid metabolism, which was modulated by dietary fat consumption, particularly PUFA intake, suggesting novel gene-nutrient interactions.


Phillips C.M.,University College Dublin | Goumidi L.,French National Institute for Agricultural Research | Bertrais S.,French National Institute for Agricultural Research | Field M.R.,Hitachi Dublin Laboratory | And 15 more authors.
Journal of Nutrition | Year: 2010

The leptin receptor (LEPR) is associated with insulin resistance, a key feature of metabolic syndrome (MetS). Gene-fatty acid interactions may affect MetS risk. The objective was to investigate the relationship among LEPR polymorphisms, insulin resistance, andMetSrisk andwhether plasma fatty acids, a biomarker of dietary fatty acids,modulate this. LEPRpolymorphisms (rs10493380, rs1137100, rs1137101, rs12067936, rs1805096, rs2025805, rs3790419, rs3790433, rs6673324, and rs8179183), biochemical measurements, and plasma fatty acid profiles were determined in the LIPGENE-SU.VI.MAX study ofMetS cases andmatched controls (n = 1754). LEPR rs3790433 GG homozygotes had increasedMetS risk compared with theminor A allele carriers [odds ratio (OR) = 1.65; 95% CI: 1.05-2.57; P = 0.028], whichmay be accounted for by their increased risk of elevated insulin concentrations (OR 2.40;95% CI: 1.28-4.50; P = 0.006) and insulin resistance (OR= 2.15; 95% CI: 1.18-3.90; P = 0.012). Low (less thanmedian) plasma (n-3) and high (n-6) PUFA status exacerbated the genetic risk conferred by GG homozygosity to hyperinsulinemia (OR 2.92-2.94) and insulin resistance (OR 3.40-3.47). Interestingly, these associationswere abolished against a high (n-3) or low (n-6) PUFA background. Importantly, we replicated some of these findings in an independent cohort. Homozygosity for theLEPRrs3790433Gallelewasassociatedwith insulin resistance,whichmaypredispose to increasedMetS risk. Novel gene-nutrient interactions between LEPR rs3790433 and PUFA suggest that these genetic influences were more evident in individuals with low plasma (n-3) or high plasma (n-6) PUFA. © 2010 American Society for Nutrition.


Knottnerus I.L.H.,Maastricht University | Knottnerus I.L.H.,Spectrum | Gielen M.,Nutrition and Toxicology Research Institute Maastricht | Gielen M.,University of Birmingham | And 5 more authors.
Stroke | Year: 2011

BACKGROUND AND PURPOSE-Results from case-control and case-case studies indicate that a positive family history of stroke (FHstroke) is an independent risk factor for lacunar stroke. Different lacunar stroke phenotypes can be distinguished on the basis of the presence of asymptomatic lacunar infarcts (aLACs), ischemic white-matter lesions, or brain microbleeds. The aim of the present study was to determine whether familial aggregation of stroke was different for lacunar stroke phenotypes. METHODS-In 157 patients with a first-ever lacunar stroke, a complete first-degree FHstroke was obtained by a standardized questionnaire and additional interview. Lacunar stroke patients were categorized successively into groups, depending on the presence of aLACs, ischemic white-matter lesions, and brain microbleeds on magnetic resonance imaging. RESULTS-Fifty-two percent of patients reported a positive FHstroke in at least one of their first-degree relatives. In younger (<65 years) probands, a high frequency of parental FHstroke (59% versus 20%, P<0.01) in those with aLACs compared with probands without aLACs was found. In multivariate analysis, the strongest associations were found for parental FHstroke (odds ratio=6.46; 95% CI=1.96 to 21.33), maternal FHstroke (odds ratio=4.00; 95% CI=1.18 to 13.56), and paternal FHstroke (odds ratio=5.40; 95% CI=1.14 to 25.61). CONCLUSIONS-A family history of stroke might be an independent risk factor for the lacunar stroke phenotype with aLACs at younger ages, suggesting a role for genetic factors in this phenotype caused by diffuse vasculopathy. © 2011 American Heart Association, Inc.


Ijzerman T.H.,Nutrition and Toxicology Research Institute Maastricht | Schaper N.C.,Maastricht University | Melai T.,Nutrition and Toxicology Research Institute Maastricht | Melai T.,Fontys University of Applied Sciences | And 3 more authors.
Diabetes Research and Clinical Practice | Year: 2012

Aim: The purpose of the present study was to distinguish the effects of both diabetes mellitus type 2 (DM2) and diabetic polyneuropathy (DPN) on mobility, muscle strength and health related quality of life (HR-QoL). Methods: DPN patients (n=98), DM2 patients without DPN (DC) (n=39) and healthy subjects (HC) (n=19) performed isometric and isokinetic lower limb muscle strength tests. Mobility was determined by a timed up and go test (TUGT), a 6 min walk test and the physical activity scale for the elderly questionnaire. HR-QoL was determined by the SF36 questionnaire. Results: DPN patients had moderate polyneuropathy. In both DPN and DC patients leg muscle strength was reduced by 30-50% compared to HC. Muscle strength was correlated with mobility tests, and reduced muscle strength as well as impaired mobility were associated with a loss of HR-Qol (all p<0.05). We did not observe major differences in muscle strength, mobility (except for the TUGT, p<0.01) and HR-QoL between diabetic patients with and without DPN. Conclusion: DM2 patients, with and without DPN, have decreased maximal muscle strength in the lower limbs and impaired mobility. These abnormalities are associated with a loss of HR-QoL. The additional effect of moderate DPN was small in our patients. © 2011 Elsevier Ireland Ltd.


Geraedts M.C.P.,Maastricht University | Geraedts M.C.P.,Nutrition and Toxicology Research Institute Maastricht | Troost F.J.,Maastricht University | Troost F.J.,Nutrition and Toxicology Research Institute Maastricht | And 14 more authors.
PLoS ONE | Year: 2011

Background: Human duodenal mucosa secretes increased levels of satiety signals upon exposure to intact protein. However, after oral protein ingestion, gastric digestion leaves little intact proteins to enter the duodenum. This study investigated whether bypassing the stomach, through intraduodenal administration, affects hormone release and food-intake to a larger extent than orally administered protein in both lean and obese subjects. Methods: Ten lean (BMI:23.0±0.7 kg/m 2) and ten obese (BMI:33.4±1.4 kg/m 2) healthy male subjects were included. All subjects randomly received either pea protein solutions (250 mg/kg bodyweight in 0.4 ml/kg bodyweight of water) or placebo (0.4 ml/kg bodyweight of water), either orally or intraduodenally via a naso-duodenal tube. Appetite-profile, plasma GLP-1, CCK, and PYY concentrations were determined over a 2 h period. After 2 h, subjects received an ad-libitum meal and food-intake was recorded. Results: CCK levels were increased at 10(p<0.02) and 20(p<0.01) minutes after intraduodenal protein administration (IPA), in obese subjects, compared to lean subjects, but also compared to oral protein administration (OPA)(p<0.04). GLP-1 levels increased after IPA in obese subjects after 90(p<0.02) to 120(p<0.01) minutes, compared to OPA. Food-intake was reduced after IPA both in lean and obese subjects (-168.9±40 kcal (p<0.01) and -298.2±44 kcal (p<0.01), respectively), compared to placebo. Also, in obese subjects, food-intake was decreased after IPA (-132.6±42 kcal; p<0.01), compared to OPA. Conclusions: Prevention of gastric proteolysis through bypassing the stomach effectively reduces food intake, and seems to affect obese subjects to a greater extent than lean subjects. Enteric coating of intact protein supplements may provide an effective dietary strategy in the prevention/treatment of obesity. © 2011 Geraedts et al.


PubMed | Nutrition and Toxicology Research Institute Maastricht
Type: Journal Article | Journal: Diabetes research and clinical practice | Year: 2012

The purpose of the present study was to distinguish the effects of both diabetes mellitus type 2 (DM2) and diabetic polyneuropathy (DPN) on mobility, muscle strength and health related quality of life (HR-QoL).DPN patients (n=98), DM2 patients without DPN (DC) (n=39) and healthy subjects (HC) (n=19) performed isometric and isokinetic lower limb muscle strength tests. Mobility was determined by a timed up and go test (TUGT), a 6 min walk test and the physical activity scale for the elderly questionnaire. HR-QoL was determined by the SF36 questionnaire.DPN patients had moderate polyneuropathy. In both DPN and DC patients leg muscle strength was reduced by 30-50% compared to HC. Muscle strength was correlated with mobility tests, and reduced muscle strength as well as impaired mobility were associated with a loss of HR-Qol (all p<0.05). We did not observe major differences in muscle strength, mobility (except for the TUGT, p<0.01) and HR-QoL between diabetic patients with and without DPN.DM2 patients, with and without DPN, have decreased maximal muscle strength in the lower limbs and impaired mobility. These abnormalities are associated with a loss of HR-QoL. The additional effect of moderate DPN was small in our patients.


PubMed | Nutrition and Toxicology Research Institute Maastricht
Type: Journal Article | Journal: The American journal of clinical nutrition | Year: 2011

Accelerated infant growth is a possible explanation for the relation between birth weight and adult diseases.The aim of this study was to estimate the heritability of infant growth and to examine whether the genetic contribution changes with increasing or decreasing birth weight and gestational age.Growth (change in weight z score) was analyzed in 522 infants from the East Flanders Prospective Twin Survey for age windows of 0-1, 1-6, 6-12, and 12-24 mo. Structural equation modeling was performed to estimate the relative importance of additive genetic, shared environmental, and unique environmental sources of variance.We showed no genetic contribution to growth in the 0-1-mo growth period. However, at later ages, the heritability of growth was high at 94% (95% CI: 90%, 96%) from 1 to 6 mo, 85% (95% CI: 80%, 89%) from 6 to 12 mo, and 86% (95% CI: 77%, 91%) in the 12-24-mo growth period. Nevertheless, in the last age window, a model without genetic factors was also statistically plausible. From 0 to 1 mo, the genetic contribution to growth was low in the average birth weight range but higher at both extremes of birth weight. The genetic contribution from 0 to 1 mo increased with increasing gestational age from 36 wk of gestation onward.This study shows that genetic factors are not important in early infant growth (0-1 mo), whereas heritability is high after 1 mo. Because many (nutritional) interventions are aimed at influencing early postnatal growth, to target long-term health, these interventions may be most successful if implemented in the first month of postnatal growth.

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