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Perez-Martinez P.,University of Cordoba, Spain | Delgado-Lista J.,University of Cordoba, Spain | Garcia-Rios A.,University of Cordoba, Spain | Mc Monagle J.,University College Dublin | And 16 more authors.
PLoS ONE | Year: 2011

Glucokinase Regulatory Protein (GCKR) plays a central role regulating both hepatic triglyceride and glucose metabolism. Fatty acids are key metabolic regulators, which interact with genetic factors and influence glucose metabolism and other metabolic traits. Omega-3 polyunsaturated fatty acids (n-3 PUFA) have been of considerable interest, due to their potential to reduce metabolic syndrome (MetS) risk. Objective: To examine whether genetic variability at the GCKR gene locus was associated with the degree of insulin resistance, plasma concentrations of C-reactive protein (CRP) and n-3 PUFA in MetS subjects. Design: Homeostasis model assessment of insulin resistance (HOMA-IR), HOMA-B, plasma concentrations of C-peptide, CRP, fatty acid composition and the GCKR rs1260326-P446L polymorphism, were determined in a cross-sectional analysis of 379 subjects with MetS participating in the LIPGENE dietary cohort. Results: Among subjects with n-3 PUFA levels below the population median, carriers of the common C/C genotype had higher plasma concentrations of fasting insulin (P = 0.019), C-peptide (P = 0.004), HOMA-IR (P = 0.008) and CRP (P = 0.032) as compared with subjects carrying the minor T-allele (Leu446). In contrast, homozygous C/C carriers with n-3 PUFA levels above the median showed lower plasma concentrations of fasting insulin, peptide C, HOMA-IR and CRP, as compared with individuals with the T-allele. Conclusions: We have demonstrated a significant interaction between the GCKR rs1260326-P446L polymorphism and plasma n-3 PUFA levels modulating insulin resistance and inflammatory markers in MetS subjects. Further studies are needed to confirm this gene-diet interaction in the general population and whether targeted dietary recommendations can prevent MetS in genetically susceptible individuals. © 2011 Perez-Martinez et al.


Perez-Martinez P.,University of Cordoba, Spain | Delgado-Lista J.,University of Cordoba, Spain | Garcia-Rios A.,University of Cordoba, Spain | Tierney A.C.,University College Dublin | And 14 more authors.
Molecular Nutrition and Food Research | Year: 2012

Scope: Several insulin receptor substrate-2 (IRS-2) polymorphisms have been studied in relation to insulin resistance and type 2 diabetes. To examine whether the genetic variability at the IRS-2 gene locus was associated with the degree of insulin resistance and plasma fatty acid levels in metabolic syndrome (MetS) subjects. Methods and results: Insulin sensitivity, insulin secretion, glucose effectiveness, plasma fatty acid composition and three IRS-2 tag-single nucleotide polymorphisms (SNPs) were determined in 452 MetS subjects. Among subjects with the lowest level of monounsaturated (MUFA) (below the median), the rs2289046 A/A genotype was associated with lower glucose effectiveness (p<0.038), higher fasting insulin concentrations (p<0.028) and higher HOMA IR (p<0.038) as compared to subjects carrying the minor G-allele (A/G and G/G). In contrast, among subjects with the highest level of MUFA (above the median), the A/A genotype was associated with lower fasting insulin concentrations and HOMA-IR, whereas individuals carrying the G allele and with the highest level of ω-3 polyunsaturated fatty acids (above the median) showed lower fasting insulin (p<0.01) and HOMA-IR (p<0.02) as compared with A/A subjects. Conclusion: The rs2289046 polymorphism at the IRS2 gene locus may influence insulin sensitivity by interacting with certain plasma fatty acids in MetS subjects. © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.


Perez-Martinez P.,University of Cordoba, Spain | Delgado-Lista J.,University of Cordoba, Spain | Garcia-Rios A.,University of Cordoba, Spain | Ferguson J.F.,University College Dublin | And 14 more authors.
American Journal of Clinical Nutrition | Year: 2011

Background: Calpain-10 protein (intracellular Ca2+-dependent cysteine protease) may play a role in glucose metabolism, pancreatic β cell function, and regulation of fhermogenesis. Several CAPN10 polymorphic sites have been studied for their potential use as risk markers for type 2 diabetes and the metabolic syndrome (MetS). Fatty acids are key metabolic regulators that may interact with genetic factors and influence glucose metabolism. Objective: The objective was to examine whether the genetic variability at the CAPN10 gene locus is associated with the degree of insulin resistance and plasma fatty acid concentrations in subjects with MetS. Design: The insulin sensitivity index, glucose effectiveness, insulin resistance [homeostasis model assessment of insulin resistance (HOMA-IR)], insulin secretion (disposition index, acute insulin response, and HOMA of β cell function), plasma fatty acid composition, and 5 CAPN10 single nucleotide polymorphisms (SNPs) were determined in a cross-sectional analysis of 452 subjects with MetS participating in the LIPGENE dietary intervention cohort. Results: The rs2953171 SNP interacted with plasma total saturated fatty acid (SFA) concentrations, which were significantly associated with insulin sensitivity (P < 0.031 for fasting insulin, P < 0.028 for HOMA-IR, and P < 0.012 for glucose effectiveness). The G/G genotype was associated with lower fasting insulin concentrations, lower HOMA-IR, and higher glucose effectiveness in subjects with low SFA concentrations (below the median) than in subjects with the minor A allele (G/A and A/A). In contrast, subjects with the G/G allele with the highest SFA concentrations (above the median) had higher fasting insulin and HOMA-IR values and lower glucose effectiveness than did subjects with the A allele. Conclusion: The rs2953171 polymorphism at the CAPN10 gene locus may influence insulin sensitivity by interacting with the plasma fatty acid composition in subjects with MetS. © 2011 American Society for Nutrition.


Garcia-Rios A.,University of Cordoba, Spain | Garcia-Rios A.,CIBER ISCIII | Delgado-Lista J.,University of Cordoba, Spain | Delgado-Lista J.,CIBER ISCIII | And 20 more authors.
Atherosclerosis | Year: 2011

Objective: To investigate whether seven common single nucleotide polymorphisms (SNPs) at the lipoprotein lipase (LPL) locus interact with total plasma fatty acids to modulate plasma lipid metabolism in metabolic syndrome (MetS) patients. Methods: Plasma fatty acid composition, plasma lipid concentrations and LPL SNPs were determined in 452 subjects with the MetS in the European LIPGENE human study and were repeated in 1754 subjects from the LIPGENE-SU.VI.MAX Study. Results: Triglycerides (TG) were lower, and HDL higher in the carriers of rs328 and rs1059611 in the SUVIMAX cohort (all P< 0.001), and these findings showed a similar, non-significant trend in LIPGENE cohort. In this last cohort, we found a gene-fatty acids interaction, as the carriers of the minor allele displayed a lower fasting TG and triglyceride rich lipoproteins-TG (TRL-TG) concentrations only when they had n-6 polyunsaturated fatty acids below the median (all P< 0.05). Moreover, subjects carrying the minor allele for rs328 SNP and with a low level of n-6 PUFA displayed higher nonesterified fatty acid (NEFA) plasma concentrations as compared with homozygous for the major allele (P= 0.034). Interestingly, the n-6 PUFA-dependent associations between those SNPs and TG metabolism were also replicated in subjects without MetS from the SU.VI.MAX cohort. Conclusion: Two genetic variations at the LPL gene (rs328 and rs1059611) influence plasma lipid concentrations and interact with plasma n-6 PUFA to modulate lipid metabolism. The knowledge of new genetic factors together with the understanding of these gene-nutrient interactions could help to a better knowledge of the pathogenesis in the MetS. © 2011 Elsevier Ireland Ltd.


Perez-Martinez P.,University of Cordoba, Spain | Perez-Martinez P.,CIBER ISCIII | Garcia-Rios A.,University of Cordoba, Spain | Garcia-Rios A.,CIBER ISCIII | And 20 more authors.
Clinical Nutrition | Year: 2013

Background & aims: Genetic background may interact with habitual dietary fat composition, and affect development of the metabolic syndrome (MetS). The phosphoenolpyruvate carboxykinase gene (PCK1) plays a significant role regulating glucose metabolism, and fatty acids are key metabolic regulators, which interact with transcription factors and influence glucose metabolism. We explored genetic variability at the PCK1 gene locus in relation to degree of insulin resistance and plasma fatty acid levels in MetS subjects. Moreover, we analyzed the PCK1 gene expression in the adipose tissue of a subgroup of MetS subjects according to the PCK1 genetic variants. Methods: Insulin sensitivity, insulin secretion, glucose effectiveness, plasma concentrations of C-peptide, fatty acid composition and three PCK1 tag-single nucleotide polymorphisms (SNPs) were determined in 443 MetS participants in the LIPGENE cohort. Results: The rs2179706 SNP interacted with plasma concentration of n-3 polyunsaturated fatty acids (n-3 PUFA), which were significantly associated with plasma concentrations of fasting insulin, peptide C, and HOMA-IR. Among subjects with n-3 PUFA levels above the population median, carriers of the C/C genotype exhibited lower plasma concentrations of fasting insulin (P=0.036) and HOMA-IR (P=0.019) as compared with C/C carriers with n-3 PUFA below the median. Moreover, homozygous C/C subjects with n-3 PUFA levels above the median showed lower plasma concentrations of peptide C as compared to individuals with the T-allele (P=0.006). Subjects carrying the T-allele showed a lower gene PCK1 expression as compared with carriers of the C/C genotype (P=0.015). Conclusions: The PCK1 rs2179706 polymorphism interacts with plasma concentration of n-3 PUFA levels modulating insulin resistance in MetS subjects. © 2012 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism.


Marsch E.,CARIM | Theelen T.L.,CARIM | Janssen B.J.A.,Maastricht University | Briede J.J.,Maastricht University | And 9 more authors.
Atherosclerosis | Year: 2016

Background: Short term dietary nitrate or nitrite supplementation has nitric oxide (NO)-mediated beneficial effects on blood pressure and inflammation and reduces mitochondrial oxygen consumption, possibly preventing hypoxia. As these processes are implicated in atherogenesis, dietary nitrate was hypothesized to prevent plaque initiation, hypoxia and inflammation. Aims: Study prolonged nitrate supplementation on atherogenesis, hypoxia and inflammation in low density lipoprotein receptor knockout mice (LDLr-/-). Methods: LDLr-/- mice were administered sodium-nitrate or equimolar sodium-chloride in drinking water alongside a western-type diet for 14 weeks to induce atherosclerosis. Plasma nitrate, nitrite and hemoglobin-bound nitric oxide were measured by chemiluminescence and electron parametric resonance, respectively. Results: Plasma nitrate levels were elevated after 14 weeks of nitrate supplementation (NaCl: 40.29 ± 2.985, NaNO3: 78.19 ± 6.837, p < 0.0001). However, prolonged dietary nitrate did not affect systemic inflammation, hematopoiesis, erythropoiesis and plasma cholesterol levels, suggesting no severe side effects. Surprisingly, neither blood pressure, nor atherogenesis were altered. Mechanistically, plasma nitrate and nitrite were elevated after two weeks (NaCl: 1.0 ± 0.2114, NaNO3: 3.977 ± 0.7371, p < 0.0001), but decreased over time (6, 10 and 14 weeks). Plasma nitrite levels even reached baseline levels at 14 weeks (NaCl: 0.7188 ± 0.1072, NaNO3: 0.9723 ± 0.1279 p = 0.12). Also hemoglobin-bound NO levels were unaltered after 14 weeks. This compensation was not due to altered eNOS activity or conversion into peroxynitrite and other RNI, suggesting reduced nitrite formation or enhanced nitrate/nitrite clearance. Conclusion: Prolonged dietary nitrate supplementation resulted in compensation of nitrite and NO levels and did not affect atherogenesis or exert systemic side effects. © 2015 The Authors.


PubMed | AMC, NUTRIM, CARIM, MUMC and Maastricht University
Type: | Journal: Atherosclerosis | Year: 2016

Short term dietary nitrate or nitrite supplementation has nitric oxide (NO)-mediated beneficial effects on blood pressure and inflammation and reduces mitochondrial oxygen consumption, possibly preventing hypoxia. As these processes are implicated in atherogenesis, dietary nitrate was hypothesized to prevent plaque initiation, hypoxia and inflammation.Study prolonged nitrate supplementation on atherogenesis, hypoxia and inflammation in low density lipoprotein receptor knockout mice (LDLr(-/-)).LDLr(-/-) mice were administered sodium-nitrate or equimolar sodium-chloride in drinking water alongside a western-type diet for 14 weeks to induce atherosclerosis. Plasma nitrate, nitrite and hemoglobin-bound nitric oxide were measured by chemiluminescence and electron parametric resonance, respectively.Plasma nitrate levels were elevated after 14 weeks of nitrate supplementation (NaCl: 40.29 2.985, NaNO3: 78.19 6.837, p < 0.0001). However, prolonged dietary nitrate did not affect systemic inflammation, hematopoiesis, erythropoiesis and plasma cholesterol levels, suggesting no severe side effects. Surprisingly, neither blood pressure, nor atherogenesis were altered. Mechanistically, plasma nitrate and nitrite were elevated after two weeks (NaCl: 1.0 0.2114, NaNO3: 3.977 0.7371, p < 0.0001), but decreased over time (6, 10 and 14 weeks). Plasma nitrite levels even reached baseline levels at 14 weeks (NaCl: 0.7188 0.1072, NaNO3: 0.9723 0.1279 p = 0.12). Also hemoglobin-bound NO levels were unaltered after 14 weeks. This compensation was not due to altered eNOS activity or conversion into peroxynitrite and other RNI, suggesting reduced nitrite formation or enhanced nitrate/nitrite clearance.Prolonged dietary nitrate supplementation resulted in compensation of nitrite and NO levels and did not affect atherogenesis or exert systemic side effects.


Bucerius J.,Maastricht University | Bucerius J.,RWTH Aachen | Vijgen G.H.E.J.,NUTRIM | Vijgen G.H.E.J.,Maastricht University | And 11 more authors.
Medicine (United States) | Year: 2015

In this study, we unravel a molecular imaging marker correlated with the known reduction of cardiovascular events (most commonly related to vulnerable plaques) in morbidly obese patients after bariatric surgery (BaS). We prospectively imaged 10 morbidly obese subjects with 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography/computed tomography before and 1 year after BaS. 18F-FDGuptake-which is enhanced in inflamed, atherosclerotic vessels and in metabolically active adipose tissues-was quantified in the carotids, pericardial adipose tissue (PAT), visceral adipose tissue (VAT), as well as brown adipose tissue (BAT). The degree of carotid inflammation was compared to lean and overweight controls. Carotid inflammation significantly declined leading to an 18F-FDG uptake comparable to the 2 control groups. Metabolic activity significantly decreased in PAT and VAT and increased in BAT. BaS leads to a normalization of carotid artery inflammation and a beneficial impact on the metabolic activity in PAT,VAT, and BAT that is related to the metabolic syndrome observed in this patient group. © 2015 Wolters Kluwer Health, Inc.


Vijgen G.,NUTRIM | Vijgen G.,Maastricht University | Van Marken Lichtenbelt W.,NUTRIM
Frontiers in Bioscience - Elite | Year: 2013

Brown adipose tissue (BAT) is physiologically present and active in adult humans. The stimulation of BAT in man can potentially increase total daily energy expenditure and is seen as a possible target to treat obesity. Altered BAT activity is also related to other diseases and therefore the therapeutic potential of BAT could reach beyond obesity. This is supported by both in vitro and in vivo reports from animal studies, describing the possible role of BAT in both physiology and pathophysiology. In addition, since the discovery of functional BAT several clinically relevant studies have been conducted in adult man. Clinical observations report BAT activity under multiple conditions, suggesting BAT could be important in the onset and/or treatment of diseases related to the metabolic syndrome, thyroid disorders, cancer and immune system dysfunction. This review highlights those diseases or syndromes in which BAT may play a role in relation to prevention, diagnosis or therapy, by translating basic research into clinical relevance.


Oomens C.W.J.,TU Eindhoven | Zenhorst W.,TU Eindhoven | Broek M.,TU Eindhoven | Poeze M.,NUTRIM | And 3 more authors.
Clinical Biomechanics | Year: 2013

Background Spine boards are used to immobilise accident victims suspected of having spinal injury. Guidelines about the maximum time patients remain on the board are often exceeded and on occasions may lead to pressure ulcers. Etiological research has shown that two processes ultimately lead to pressure ulcers:"Ischemic damage" which takes several hours to initiate and "deformation damage" at high strains. The latter process is very quick and the first signs of cell damage are already evident within minutes. Thus in order to minimise the risk of pressure ulcer development during prolonged loading, a new soft-layered long spine board has been designed. Methods A subject specific numerical approach has been adopted to evaluate the prototype spine board in comparison to a conventional spine board, with reference to the estimated strains in the soft tissues adjacent to the sacrum in the supine position. The model geometry is derived from magnetic resonance images of three human volunteers in an unloaded situation. The loaded images are used to "tune" the material parameters of skin, fat and muscle. The prediction of the deformed contours on the soft-layered board is used to validate the model. Findings Comparison of the internal strains in muscle tissue near the spine showed that internal strains on the soft-layered board are reduced and maximum strains are considerably less than the threshold at which deformation damage is possible. By contrast, on the rigid spine board this threshold is exceeded in all cases. Interpretation The prototype comfort board is able to reduce the risk for deformation damage and thus reduces the risk of developing pressure ulcers. © 2013 Elsevier Ltd.

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