Antonio Camargo

Hospital Universitario Reina Sofía, Córdoba, Andalusia, Spain

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Publications (17)80.01 Total impact

  • Article: The antioxidants in oils heated at frying temperature, whether natural or added, could protect against postprandial oxidative stress in obese people.
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    ABSTRACT: We have investigated the effects of the intake of oils heated at frying temperature in order to find an oil model for deep-frying that prevents postprandial oxidative stress. Twenty obese people received four breakfasts following a randomised crossover design consisting of different oils (virgin olive oil (VOO), sunflower oil (SFO), and a mixed seed oil (SFO/canola oil) with added dimethylpolysiloxane (SOX) or natural antioxidants from olives (SOP)), which were subjected to 20 heating cycles. The intake of SFO-breakfast reduced plasma GSH levels and the GSH/GSSG ratio, increased protein carbonyl levels, and induced a higher gene expression of the different NADPH-oxidase subunits, Nrf2-Keap1 activation, gene expression of the antioxidant enzymes in peripheral blood mononuclear cells and antioxidant plasma activities than the intake of the breakfasts prepared with VOO, SOP and SOX. Oils with phenolic compounds, whether natural (VOO) or artificially added (SOP), or with artificial antioxidant (SOX), could reduce postprandial oxidative stress compared with sunflower oil.
    Food Chemistry 06/2013; 138(4):2250-9. · 3.65 Impact Factor
  • Article: Antioxidant system response is modified by dietary fat in adipose tissue of metabolic syndrome patients.
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    ABSTRACT: Metabolic syndrome (MetS) is associated with high oxidative stress, which is caused by an increased expression of NADPH-oxidase and a decreased expression of antioxidant enzymes in the adipose tissue. Our aim was to evaluate whether the quality and quantity of dietary fat can modify that process. A randomized, controlled trial conducted within the LIPGENE study assigned MetS patients to one of four diets for 12 wk each: (i) high-saturated fatty acid (HSFA), (ii) high-monounsaturated fatty acid (HMUFA), (iii) and (iv) two low-fat, high-complex carbohydrate diet supplemented with n-3 polyunsaturated fatty acids (LFHCC n3), or placebo (LFHCC). A fat challenge reflecting the same fatty acid composition as the original diets was conducted post-intervention. The intake of an HSFA meal induced a higher postprandial increase in gp91phox and p67phox mRNA levels than after the intake of HMUFA, LFHCC and LFHCC n-3 meals (all p-values<0.05). The postprandial decrease in CAT, GPXs and TXNRD1 mRNA levels after the HSFA meal intake was higher than after the intake of HMUFA, LFHCC and LFHCC n-3 meals (all p-values<0.05). The intake of an HSFA meal induced a higher postprandial increase in KEAP1 mRNA levels than after the consumption of the HMUFA (P=.007) and LFHCC n-3 (P=.001) meals. Our study demonstrated that monounsaturated fat consumption reduces oxidative stress as compared to saturated fat by inducing higher postprandial antioxidant response in adipose tissue, and thus, replacing SFA for MUFA may be an effective dietary strategy to reduce the oxidative stress in MetS patients and its pathophysiological consequences.
    The Journal of nutritional biochemistry 05/2013; · 4.29 Impact Factor
  • Article: Lipid metabolism after an oral fat test meal is affected by age-associated features of metabolic syndrome, but not by age.
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    ABSTRACT: OBJECTIVE: Postprandial lipemia influences the development of atherosclerosis. Age has been defined as a regulating factor of the extent of postprandial lipemia, but its independence of other age-associated phenotypic features, such as metabolic syndrome, has not been fully elucidated. METHODS: To investigate if age is an independent factor influencing postprandial lipemia, we compared the lipemic response to a rich fatty meal (60% fat) of 88 healthy young men (<30 years old) and 97 older participants (77 metabolic syndrome patients aged > 40; and 20 healthy people > 65) (all ApoE3/E3), at fasting state and at 2nd and 4th postprandial hours. RESULTS: We didn't find differences between the healthy young men and the healthy elderly. The metabolic syndrome patients displayed a higher postprandial TG area below the curve than the other two cohorts p < 0.001. ANOVA for repeated measurements confirmed that these differences were significant at every time-point (fasting, 2 h and 4 h). Concomitant higher responses for Large and Small TRL-carried TG and Chol were found in these metabolic syndrome patients. Interestingly, the most significant differences were found for Small-TRL-carried particles, which suggest that this fact may be mainly due to impaired lipid clearance. CONCLUSION: Metabolic syndrome may account for the differences in postprandial lipemia that have been attributed to age. In our study, there were no significant differences in postprandial lipemia between a young population (mean age 22.6 years) and a healthy people >65 years one (67.2 years) without metabolic syndrome.
    Atherosclerosis 10/2012; · 3.79 Impact Factor
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    Article: Gene-nutrient interactions on the phosphoenolpyruvate carboxykinase influence insulin sensitivity in metabolic syndrome subjects.
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    ABSTRACT: 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.
    Clinical nutrition (Edinburgh, Scotland) 10/2012; · 3.27 Impact Factor
  • Article: Postprandial changes in the proteome are modulated by dietary fat in patients with metabolic syndrome.
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    ABSTRACT: Metabolic syndrome is a multicomponent disorder whose etiology is the result of a complex interaction between genetic, metabolic and environmental factors including dietary habits. Our aim was to identify proteome-diet interactions during the postprandial state after the acute intake of four meals with different qualities of fat in the proteome of peripheral blood mononuclear cells. A randomized controlled trial conducted within the LIPGENE study assigned 39 metabolic syndrome patients to one of four meals: a high-saturated-fatty-acid (HSFA) meal, a high-monounsaturated-fatty-acid (HMUFA) meal and two high-polyunsaturated-fatty-acid (from walnut) (HPUFA) meals supplemented with n-3 PUFA or placebo. We analyzed the postprandial changes in the whole proteome of both nuclear and cytoplasmic fractions of peripheral blood mononuclear cells by two-dimensional proteomics. Twenty-three proteins were differentially expressed. HSFA intake caused the postprandial increase of proteins responding to oxidative stress (HSPA1A, PDIA3 and PSME1) and DNA damage (SMC6), whereas HMUFA intake led to the up-regulation of HSPA1A and PDIA3. HPUFA meal supplementation with n-3 PUFA produced peroxisomal beta-oxidation inhibition by down-regulation of ECH1, a process related to insulin signaling improvement. In conclusion, HSFA meal intake causes deleterious postprandial changes in the proteome in terms of DNA damage and procoagulant state, which reflect a higher postprandial oxidative stress after HSFA meal intake as compared to intake of HMUFA and HPUFA meals. Moreover, the addition of long-chain n-3 PUFA to an HPUFA meal may improve insulin signaling and exerts an anti-inflammatory effect when compared to an HPUFA meal.
    The Journal of nutritional biochemistry 09/2012; · 4.29 Impact Factor
  • Article: Dietary fat modifies the postprandial inflammatory state in subjects with metabolic syndrome: the LIPGENE study.
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    ABSTRACT: Our aim was to investigate whether the inflammatory state associated to metabolic syndrome (MetS) patients is affected by diets with different fat quality and quantity. Seventy-five subjects from LIPGENE cohort were included in this feeding trial and randomly assigned to one of four diets: high saturated fatty acids (HSFA); high monounsaturated fatty acids (HMUFA) and two low-fat, high complex carbohydrate (LFHCC) diets, supplemented with long-chain n-3 polyunsaturated fatty acids (LFHCC n-3) or placebo (LFHCC), for 12 weeks each. A postprandial fat challenge, reflecting the intervention dietary fat composition, was conducted post-intervention. The HMUFA diet significantly reduced postprandial nuclear transcription factor-kappaB (NF-kB) activity and the nuclear p65 protein levels relative to fasting values (p < 0.05). Furthermore, we observed a postprandial decrease in this protein with the HMUFA diet compared with the HSFA and LFHCC diets (p < 0.05). The postprandial response of inhibitory molecule from NF-kB mRNA levels increased with the HMUFA diet compared with the HSFA and LFHCC n-3 diets (p < 0.05). Postprandial tumor necrosis factor-α and Metalloproteinase 9 mRNA levels were also reduced after the HMUFA diet compared with the HSFA diet (p < 0.05). Our results indicate that the long-term consumption of a healthy diet model with HMUFA attenuates the postprandial inflammatory state associated with MetS.
    Molecular Nutrition & Food Research 06/2012; 56(6):854-65. · 4.30 Impact Factor
  • Article: Effects of rs7903146 variation in the Tcf7l2 gene in the lipid metabolism of three different populations.
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    ABSTRACT: TCF7L2 rs7903146 is an important genetic factor predicting type 2 diabetes (T2DM) which has also been linked to higher cardiovascular risk. To date, there is little information about the additional impact of this single nucleotide polymorphism (SNP) beyond glucose metabolism. We studied whether rs7903146 influenced postprandial lipid metabolism in three different populations (healthy young men, metabolic syndrome (MetS) patients and elderly persons). Eighty-eight healthy males were submitted to a single saturated fatty acid-rich test meal. Additionally, 110 middle-aged MetS patients and 20 healthy elderly persons (≥ 65 years) were submitted to three different dietary models followed by test meals. Minor allele homozygotes for rs7903146 showed a worse postprandial lipemia profile in young males, as seen by a lower HDL-cholesterol and Apo A1 concentration during the postprandial lipemia and a trend towards higher triglycerides (TG), than the other genotypes. In healthy elderly persons, carriers of the minor allele showed higher total cholesterol, LDL-cholesterol, Apo B and TG in the fasting state, and a higher postprandial area under the curve for total cholesterol, Apo B, small-triglyceride rich lipoprotein (TRL) cholesterol and small-(TRL) triglycerides. These results were accompanied by differential changes in adipokines. We did not observe any influence of rs7903146 on the postprandium of MetS patients. Healthy young males and elderly persons who are carriers of the mutant allele for rs7903146 have an impaired postprandial lipid metabolism that may be mediated by an alteration in adipokine regulation, and may be related to the higher cardiovascular risk observed in these persons. ClinicalTrials.gov NCT00429195.
    PLoS ONE 01/2012; 7(8):e43390. · 4.09 Impact Factor
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    Article: Postprandial inflammatory response in adipose tissue of patients with metabolic syndrome after the intake of different dietary models.
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    ABSTRACT: Dysfunctional adipose tissue may be an important trigger of molecular inflammatory pathways that cause cardiovascular diseases. Our aim was to determine whether the specific quality and quantity of dietary fat produce differential postprandial inflammatory responses in adipose tissue from metabolic syndrome (MetS) patients. A randomized, controlled trial conducted within the LIPGENE study assigned MetS patients to 1 of 4 diets: (i) high-saturated fatty acid (HSFA), (ii) high-monounsaturated fatty acid (HMUFA), (iii) low-fat, high-complex carbohydrate diet supplemented with n-3 polyunsaturated fatty acids (PUFA) (LFHCC n-3), and (iv) low-fat, high-complex carbohydrate diet supplemented with placebo (LFHCC), for 12 wk each. A fat challenge reflecting the fatty acid composition as the original diets was conducted post-intervention. We found that p65 gene expression is induced in adipose tissue (p=0.003) at the postprandial state. In addition, IκBα (p<0.001), MCP-1 (p<0.001) and IL-1β (p<0.001) gene expression was equally induced in the postprandial state, regardless of the quality and quantity of the dietary fat. Notably, IL-6 transcripts were only detected in the postprandial state. Our results indicate that individuals with MetS typically exhibit exacerbated adipose tissue postprandial inflammatory responses, which seem to be independent of the quality and quantity of dietary fat.
    Molecular Nutrition & Food Research 12/2011; 55(12):1759-70. · 4.30 Impact Factor
  • Article: Expression of proinflammatory, proatherogenic genes is reduced by the Mediterranean diet in elderly people.
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    ABSTRACT: Ageing is an important determinant of atherosclerosis development rate, mainly by the creation of a chronic low-grade inflammation. Diet, and particularly its fat content, modulates the inflammatory response in the fasting and postprandial states. Our aim was to study the effects of dietary fat on the expression of genes related to inflammation (NF-κB, monocyte chemoattractant protein 1 (MCP-1), TNF-α and IL-6) and plaque stability (matrix metalloproteinase 9, MMP-9) during the postprandial state of twenty healthy, elderly people who followed three diets for 3 weeks each: (1) Mediterranean diet (Med Diet) enriched in MUFA with virgin olive oil; (2) SFA-rich diet; and (3) low-fat, high-carbohydrate diet enriched in n-3 PUFA (CHO-PUFA diet) by a randomised crossover design. At the end of each period, after a 12-h fast, the subjects received a breakfast with a composition similar to the one when the dietary period ended. In the fasting state, the Med Diet consumption induced a lower gene expression of the p65 subunit of NF-κB compared with the SFA-rich diet (P = 0·019). The ingestion of the Med Diet induced a lower gene postprandial expression of p65 (P = 0·033), MCP-1 (P = 0·0229) and MMP-9 (P = 0·041) compared with the SFA-rich diet, and a lower gene postprandial expression of p65 (P = 0·027) and TNF-α (P = 0·047) compared with the CHO-PUFA diet. Direct plasma quantification mostly reproduced the findings. Our data suggest that consumption of a Med Diet reduces the postprandial inflammatory response in mononuclear cells compared with the SFA-rich and CHO-PUFA diets in elderly people. These findings may be partly responsible for the lower CVD risk found in populations with a high adherence to the Med Diet.
    The British journal of nutrition 11/2011; 108(3):500-8. · 3.45 Impact Factor
  • Article: NOS3 Glu298Asp polymorphism interacts with virgin olive oil phenols to determine the postprandial endothelial function in patients with the metabolic syndrome.
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    ABSTRACT: Glu298Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene (NOS3) has been characterized as a risk factor of hypertension and coronary artery disease. Previous studies suggest that the higher risk observed in T allele carriers is due to endothelial dysfunction associated with a lower eNOS activity and that acute consumption of phenol-rich olive oil ameliorates postprandial endothelial dysfunction by reducing oxidative stress and increasing nitric oxide bioavailability. Nevertheless, how these facts may interact in a population with altered endothelial function such as metabolic syndrome patients remains unknown. The objective of the study was to evaluate whether the presence of NOS3 Glu298Asp polymorphism interacts with the phenol content of virgin olive oil (VOO) to influence postprandial endothelial function. Fifty-seven subjects with metabolic syndrome received three breakfasts based on VOO with different phenolic content. Baseline, incremental area under the curve, peak, and maximum parameters of postocclusive skin reactive hyperemia (PORH) were evaluated by laser Doppler, and the nitrate/nitrite [NO((x))] and eNOS concentrations were obtained during fasting and postprandially. A gene-diet interaction was found on maximum PORH and NO((x)) (P = 0.039 and P = 0.043, respectively). TT subjects showed lower values of eNOS, NO((x)), and maximum PORH as compared with GG and GT subjects, especially in the postprandial measurements (all P < 0.05). However, most of these differences were attenuated when high-phenol VOO was consumed. In a population with a compromised endothelial function, concentrations of phenols in dietary VOO interact with NOS3 Glu298Asp to ameliorate the endothelial dysfunction associated to the TT genotype.
    The Journal of clinical endocrinology and metabolism 08/2011; 96(10):E1694-702. · 6.50 Impact Factor
  • Article: Mediterranean diet supplemented with coenzyme Q10 induces postprandial changes in p53 in response to oxidative DNA damage in elderly subjects.
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    ABSTRACT: Coenzyme Q10 (CoQ) is a powerful antioxidant that reduces oxidative stress. We explored whether the quality of dietary fat alters postprandial oxidative DNA damage and whether supplementation with CoQ improves antioxidant capacity by modifying the activation/stabilization of p53 in elderly subjects. In this crossover study, 20 subjects were randomly assigned to receive three isocaloric diets during 4 weeks each: (1) Mediterranean diet (Med diet), (2) Mediterranean diet supplemented with CoQ (Med+CoQ diet), and (3) saturated fatty acid-rich diet (SFA diet). Levels of mRNAs were determined for p53, p21, p53R2, and mdm2. Protein levels of p53, phosphorylated p53 (Ser20), and monoubiquitinated p53 were also measured, both in cytoplasm and nucleus. The extent of DNA damage was measured as plasma 8-OHdG. SFA diet displayed higher postprandial 8-OHdG concentrations, p53 mRNA and monoubiquitinated p53, and lower postprandial Mdm2 mRNA levels compared with Med and Med+CoQ diets (p < 0.05). Moreover, Med+CoQ diet induced a postprandial decrease of cytoplasmatic p53, nuclear p-p53 (Ser20), and nuclear and cytoplasmatic monoubiquitinated p53 protein (p < 0.05). In conclusion, Med+CoQ diet improves oxidative DNA damage in elderly subjects and reduces processes of cellular oxidation. Our results suggest a starting point for the prevention of oxidative processes associated with aging.
    Age 03/2011; 34(2):389-403. · 6.28 Impact Factor
  • Article: The insulin sensitivity response is determined by the interaction between the G972R polymorphism of the insulin receptor substrate 1 gene and dietary fat.
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    ABSTRACT: Insulin resistance, a condition associated with type 2 diabetes mellitus, results from the interaction of environmental and genetic factors. The aim of this study was to explore the influence of the G972R polymorphism at the insulin receptor substrate 1 gene on insulin sensitivity in a healthy young population. Furthermore, we examined whether the presence of this single nucleotide polymorphism (SNP; GR or GG) interacts with dietary fat to modulate insulin sensitivity. Fifty-nine healthy volunteers consumed three diets during 4 wk each following a randomized crossover design: a saturated fatty acid diet, a low-fat and high carbohydrate (CHO) diet or a MUFA diet. For each diet, we investigated peripheral insulin sensitivity with the insulin suppression test. Steady-state plasma glucose and plasma-free fatty acids concentrations were significantly lower in GR subjects after the intake of a CHO diet, than did homozygous GG subjects (p<0.05). However, no differences were observed after consuming the two other diets. Insulin sensitivity increased in GR subjects for the G972R polymorphism at the insulin receptor substrate 1 gene locus, after intake of a CHO diet. Increased knowledge of how these and other genes influence insulin sensitivity should increase the understanding of personalized nutrition.
    Molecular Nutrition & Food Research 02/2011; 55(2):328-35. · 4.30 Impact Factor
  • Article: APOA1 and APOA4 gene polymorphisms influence the effects of dietary fat on LDL particle size and oxidation in healthy young adults.
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    ABSTRACT: We investigated whether APOA1 and APOA4 genotypes interact with diet to determine changes in LDL size and their susceptibility to oxidative modifications. A total of 97 healthy volunteers each consumed 3 diets for 4 wk: a SFA diet (38% fat, 20% SFA) followed by a low-fat and high-carbohydrate (CHO) diet (30% fat, 55% carbohydrate) or a monounsaturated fatty acid (MUFA) diet (38% fat, 22% MUFA) following a randomized crossover design. For each diet, we determined susceptibility to oxidative modifications and LDL size. To investigate the combined effects of the APOA1 G-76A and APOA4 Thr347Ser single nucleotide polymorphisms (SNP), we defined 4 combined genotype groups: GG/ThrThr, GG/ThrSer, GA/ThrThr, and GA/ThrSer. After participants consumed the CHO diet, there was a significant decrease in LDL size with respect to high-fat diets in GG homozygotes for the APOA1 G-76A SNP. However, LDL size did not differ in GA carriers among participants consuming the 3 diets. Carriers of the A allele for this polymorphism had smaller LDL size as well as increased susceptibility to oxidation after the SFA diet than the GG homozygous. Moreover, the interaction between the APO A1 and APOA4 genotypes revealed that individuals with the GA/ThrSer genotype had larger LDL particle size during consumption of the MUFA diet than when they consumed the CHO diet. No differences in LDL oxidation were found in this analysis. Our study supports the concept that SNP in APOA1and APOA4 genes influences atherogenic characteristics of LDL particles in response to diet.
    Journal of Nutrition 02/2010; 140(4):773-8. · 3.92 Impact Factor
  • Article: ABCA1 gene variants regulate postprandial lipid metabolism in healthy men.
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    ABSTRACT: Genetic variants of ABCA1, an ATP-binding cassette (ABC) transporter, have been linked to altered atherosclerosis progression and fasting lipid concentration, mainly high-density lipoproteins and apolipoprotein A1; however, results from different studies have been inconsistent. To further characterize the effects of ABCA1 variants in human postprandial lipid metabolism, we studied the influence of 3 single nucleotide polymorphisms (i27943 [rs2575875]; i48168 [rs4149272]; R219K [rs2230806]) in the postprandial lipemia of 88 normolipidemic young men who were given a fatty meal. For i27943 and i48168 single nucleotide polymorphisms, fasting and postprandial values of apolipoprotein A1 were higher and postprandial lipemia was much lower in homozygotes for the major alleles, total triglycerides in plasma, and large triglyceride-rich lipoprotein triglycerides. These persons also showed a higher apolipoprotein A1/apolipoprotein B ratio. Major allele homozygotes for i48168 and i27943 showed additionally higher high-density lipoproteins and lower postprandial apolipoprotein B. Our work shows that major allele homozygotes for ABCA1 single nucleotide polymorphisms i27943 and i48168 have a lower postprandial response as compared to minor allele carriers. This finding may further characterize the role of ABCA1 in lipid metabolism.
    Arteriosclerosis Thrombosis and Vascular Biology 02/2010; 30(5):1051-7. · 6.37 Impact Factor
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    Article: Gene expression changes in mononuclear cells in patients with metabolic syndrome after acute intake of phenol-rich virgin olive oil.
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    ABSTRACT: Previous studies have shown that acute intake of high-phenol virgin olive oil reduces pro-inflammatory, pro-oxidant and pro-thrombotic markers compared with low phenols virgin olive oil, but it still remains unclear whether effects attributed to its phenolic fraction are exerted at transcriptional level in vivo. To achieve this goal, we aimed at identifying expression changes in genes which could be mediated by virgin olive oil phenol compounds in the human. Postprandial gene expression microarray analysis was performed on peripheral blood mononuclear cells during postprandial period. Two virgin olive oil-based breakfasts with high (398 ppm) and low (70 ppm) content of phenolic compounds were administered to 20 patients suffering from metabolic syndrome following a double-blinded, randomized, crossover design. To eliminate the potential effect that might exist in their usual dietary habits, all subjects followed a similar low-fat, carbohydrate rich diet during the study period. Microarray analysis identified 98 differentially expressed genes (79 underexpressed and 19 overexpressed) when comparing the intake of phenol-rich olive oil with low-phenol olive oil. Many of these genes seem linked to obesity, dyslipemia and type 2 diabetes mellitus. Among these, several genes seem involved in inflammatory processes mediated by transcription factor NF-kappaB, activator protein-1 transcription factor complex AP-1, cytokines, mitogen-activated protein kinases MAPKs or arachidonic acid pathways. This study shows that intake of virgin olive oil based breakfast, which is rich in phenol compounds is able to repress in vivo expression of several pro-inflammatory genes, thereby switching activity of peripheral blood mononuclear cells to a less deleterious inflammatory profile. These results provide at least a partial molecular basis for reduced risk of cardiovascular disease observed in Mediterranean countries, where virgin olive oil represents a main source of dietary fat. Admittedly, other lifestyle factors are also likely to contribute to lowered risk of cardiovascular disease in this region.
    BMC Genomics 01/2010; 11:253. · 4.07 Impact Factor
  • Article: Nitrate signaling by the regulatory gene NIT2 in Chlamydomonas.
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    ABSTRACT: Positive signaling by nitrate in its assimilation pathway has been studied in Chlamydomonas reinhardtii. Among >34,000 lines generated by plasmid insertion, 10 mutants were unable to activate nitrate reductase (NIA1) gene expression and had a Nit(-) (no growth in nitrate) phenotype. Each of these 10 lines was mutated in the nitrate assimilation-specific regulatory gene NIT2. The complete NIT2 cDNA sequence was obtained, and its deduced amino acid sequence revealed GAF, Gln-rich, Leu zipper, and RWP-RK domains typical of transcription factors and transcriptional coactivators associated with signaling pathways. The predicted Nit2 protein sequence is structurally related to the Nin (for nodule inception) proteins from plants but not to NirA/Nit4/Yna proteins from fungi and yeast. NIT2 expression is negatively regulated by ammonium and is optimal in N-free medium with no need for the presence of nitrate. However, intracellular nitrate is required to allow Nit2 to activate the NIA1 promoter activity. Nit2 protein was expressed in Escherichia coli and shown to bind to specific sequences at the NIA1 gene promoter. Our data indicate that NIT2 is a central regulatory gene required for nitrate signaling on the Chlamydomonas NIA1 gene promoter and that intracellular nitrate is needed for NIT2 function and to modulate NIA1 transcript levels.
    The Plant Cell 11/2007; 19(11):3491-503. · 8.99 Impact Factor
  • Article: Ammonium transporter genes in Chlamydomonas: the nitrate-specific regulatory gene Nit2 is involved in Amt1;1 expression.
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    ABSTRACT: Ammonium transport is a key process in nitrogen metabolism. In the green alga Chlamydomonas, we have characterized molecularly the largest family of ammonium transporters (AMT1) so far described consisting of eight members. CrAmt1 genes have an interesting transcript structure with some very small exons. Differential expression patterns were found for each CrAmt1 gene in response to the nitrogen source by using Real Time PCR. These expression patterns were similar under high and low CO2 atmosphere. CrAmt1;1 expression was characterized in detail. It was repressed in both ammonium and nitrate medium, and strongly expressed in nitrogen-free media. Treatment with a Glutamine synthetase inhibitor released partially repression in ammonium and nitrate suggesting that ammonium and its derivatives participate in the observed repressing effects. By studying CrAmt1;1 expression in mutants deficient at different steps of the nitrate assimilation pathway, it has been shown that nitrate has a double negative effect on this gene expression; one related to its reduction to ammonium, and a second one by itself. This second effect of nitrate was dependent on the functionality of the regulatory gene Nit2, specific for nitrate assimilation. Thus, NIT2 would have a dual role on gene expression: the well-known positive one on nitrate assimilation and a novel negative one on Amt1;1 regulation.
    Plant Molecular Biology 01/2005; 56(6):863-78. · 4.15 Impact Factor

Institutions

  • 2010–2012
    • Hospital Universitario Reina Sofía
      Córdoba, Andalusia, Spain
    • Instituto Maimónides de Investigación Biomédica de Córdoba
      Córdoba, Andalusia, Spain
  • 2011
    • Instituto de Salud Carlos III
      Madrid, Madrid, Spain
  • 2007
    • Universidad Católica de Córdoba
      Córdoba, Provincia de Cordoba, Argentina