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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. Source

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. Source

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. Source

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. Source

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. Source

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