17 results on '"Sonia, García-Carpintero"'
Search Results
2. Spatial and Temporal Protein Modules Signatures Associated with Alzheimer Disease in 3xTg-AD Mice Are Restored by Early Ubiquinol Supplementation
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Emilio Llanos-González, Francisco J. Sancho-Bielsa, Javier Frontiñán-Rubio, Yoana Rabanal-Ruíz, Sonia García-Carpintero, Eduardo Chicano, Isabel Úbeda-Banon, Alicia Flores-Cuadrado, Lydia Giménez-Llort, Francisco Javier Alcaín, Juan Ramón Peinado, and Mario Durán-Prado
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3xTg-AD mice ,Alzheimer’s disease ,coenzyme Q10 ,MALDI-imaging ,mass spectrometry ,ubiquinol ,Therapeutics. Pharmacology ,RM1-950 - Abstract
Despite its robust proteopathic nature, the spatiotemporal signature of disrupted protein modules in sporadic Alzheimer’s disease (AD) brains remains poorly understood. This considered oxidative stress contributes to AD progression and early intervention with coenzyme Q10 or its reduced form, ubiquinol, delays the progression of the disease. Using MALDI–MSI and functional bioinformatic analysis, we have developed a protocol to express how deregulated protein modules arise from hippocampus and cortex in the AD mice model 3xTG-AD in an age-dependent manner. This strategy allowed us to identify which modules can be efficiently restored to a non-pathological condition by early intervention with ubiquinol. Indeed, an early deregulation of proteostasis-related protein modules, oxidative stress and metabolism has been observed in the hippocampus of 6-month mice (early AD) and the mirrored in cortical regions of 12-month mice (middle/late AD). This observation has been validated by IHC using mouse and human brain sections, suggesting that these protein modules are also affected in humans. The emergence of disrupted protein modules with AD signature can be prevented by early dietary intervention with ubiquinol in the 3xTG-AD mice model.
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- 2023
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3. Interplay Between Mitochondrial Oxidative Disorders and Proteostasis in Alzheimer’s Disease
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Emilio Llanos-González, Ángel Andres Henares-Chavarino, Cristina María Pedrero-Prieto, Sonia García-Carpintero, Javier Frontiñán-Rubio, Francisco Javier Sancho-Bielsa, Francisco Javier Alcain, Juan Ramón Peinado, Yoana Rabanal-Ruíz, and Mario Durán-Prado
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Alzheimer’s disease ,autophagy ,endoplasmic reticulum stress ,oxidative stress ,proteasomal degradation ,unfolded protein response ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Although the basis of Alzheimer’s disease (AD) etiology remains unknown, oxidative stress (OS) has been recognized as a prodromal factor associated to its progression. OS refers to an imbalance between oxidant and antioxidant systems, which usually consist in an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) which overwhelms the intrinsic antioxidant defenses. Due to this increased production of ROS and RNS, several biological functions such as glucose metabolism or synaptic activity are impaired. In AD, growing evidence links the ROS-mediated damages with molecular targets including mitochondrial dynamics and function, protein quality control system, and autophagic pathways, affecting the proteostasis balance. In this scenario, OS should be considered as not only a major feature in the pathophysiology of AD but also a potential target to combat the progression of the disease. In this review, we will discuss the role of OS in mitochondrial dysfunction, protein quality control systems, and autophagy associated to AD and suggest innovative therapeutic strategies based on a better understanding of the role of OS and proteostasis.
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- 2020
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4. Ubiquinol Supplementation Improves Gender-Dependent Cerebral Vasoreactivity and Ameliorates Chronic Inflammation and Endothelial Dysfunction in Patients with Mild Cognitive Impairment
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Sonia García-Carpintero, Javier Domínguez-Bértalo, Cristina Pedrero-Prieto, Javier Frontiñán-Rubio, Mariano Amo-Salas, Mario Durán-Prado, Eloy García-Pérez, Julia Vaamonde, and Francisco J. Alcain
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coenzyme Q10 ,breath holding index ,LPS ,endothelial necrosis ,mild cognitive impairment ,Therapeutics. Pharmacology ,RM1-950 - Abstract
Ubiquinol can protect endothelial cells from multiple mechanisms that cause endothelial damage and vascular dysfunction, thus contributing to dementia. A total of 69 participants diagnosed with mild cognitive impairment (MCI) received either 200 mg/day ubiquinol (Ub) or placebo for 1 year. Cognitive assessment of patients was performed at baseline and after 1 year of follow-up. Patients’ cerebral vasoreactivity was examined using transcranial Doppler sonography, and levels of Ub and lipopolysaccharide (LPS) in plasma samples were quantified. Cell viability and necrotic cell death were determined using the microvascular endothelial cell line bEnd3. Coenzyme Q10 (CoQ) levels increased in patients supplemented for 1 year with ubiquinol versus baseline and the placebo group, although higher levels were observed in male patients. The higher cCoQ concentration in male patients improved cerebral vasoreactivity CRV and reduced inflammation, although the effect of Ub supplementation on neurological improvement was negligible in this study. Furthermore, plasma from Ub-supplemented patients improved the viability of endothelial cells, although only in T2DM and hypertensive patients. This suggests that ubiquinol supplementation could be recommended to reach a concentration of 5 μg/mL in plasma in MCI patients as a complement to conventional treatment.
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- 2021
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5. CoQ10 reduces glioblastoma growth and infiltration through proteome remodeling and inhibition of angiogenesis and inflammation
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Javier Frontiñán-Rubio, Emilio Llanos-González, Sonia García-Carpintero, Juan Ramón Peinado, Inmaculada Ballesteros-Yáñez, Margarita Villar Rayo, José de la Fuente, Víctor M. Pérez-García, Luis A. Perez-Romasanta, Marcos Malumbres, Francisco J. Alcaín, Mario Durán-Prado, Junta de Comunidades de Castilla-La Mancha, Universidad de Castilla La Mancha, Ministerio de Economía y Competitividad (España), and European Commission
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Inflammation ,Cancer Research ,Coenzima Q10 ,Invasión ,Oncology ,Invasion ,Inflamación ,Angiogénesis ,Molecular Medicine ,Coenzyme Q10 ,General Medicine ,Angiogenesis ,Glioblastoma - Abstract
[Purpose] Most monotherapies available against glioblastoma multiforme (GBM) target individual hallmarks of this aggressive brain tumor with minimal success. In this article, we propose a therapeutic strategy using coenzyme Q10 (CoQ10) as a pleiotropic factor that crosses the blood–brain barrier and accumulates in cell membranes acting as an antioxidant, and in mitochondrial membranes as a regulator of cell bioenergetics and gene expression., [Methods] Xenografts of U251 cells in nu/nu mice were used to assay tumor growth, hypoxia, angiogenesis, and inflammation. An orthotopic model was used to explore microglial infiltration, tumor growth, and invasion into the brain parenchyma. Cell proliferation, migration, invasion, proteome remodeling, and secretome were assayed in vitro. Conditioned media were used to assay angiogenesis, monocyte chemoattraction, and differentiation into macrophages in vitro., [Results] CoQ10 treatment decreased tumor volume in xenografts and orthotopic models, although its effect on tumor cell proliferation was not direct. Tumors from mice treated with CoQ10 were less hypoxic and vascularized, having less infiltration from inflammatory cells. Treatment-induced downregulation of HIF-1α and NF-kB led to a complete remodeling of the tumor cells proteome and secretome, impacting angiogenesis, monocyte infiltration, and their differentiation into macrophages. Besides, tumor cell migration and invasion were drastically restricted by mechanisms involving modulation of the actin cytoskeleton and downregulation of matrix metalloproteases (MMPs)., [Conclusions] CoQ10 has a pleiotropic effect on GBM growth, targeting several hallmarks simultaneously. Thus, its integration into current treatments of this fatal disease should be considered., This work has been supported by Grants 220020351 (James S. MacDonnell Foundation), GE20112221 (Universidad de Castilla-La Mancha), PPII-2014–010-P (Junta de Comunidades de Castilla-La Mancha), MTM2015-71200-R (MINECO-FEDER), and SAF2016-79311-R (MINECO-FEDER).
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- 2022
6. CoQ
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Javier, Frontiñán-Rubio, Emilio, Llanos-González, Sonia, García-Carpintero, Juan Ramón, Peinado, Inmaculada, Ballesteros-Yáñez, Margarita Villar, Rayo, José, de la Fuente, Víctor M, Pérez-García, Luis A, Perez-Romasanta, Marcos, Malumbres, Francisco J, Alcaín, and Mario, Durán-Prado
- Abstract
Most monotherapies available against glioblastoma multiforme (GBM) target individual hallmarks of this aggressive brain tumor with minimal success. In this article, we propose a therapeutic strategy using coenzyme QXenografts of U251 cells in nu/nu mice were used to assay tumor growth, hypoxia, angiogenesis, and inflammation. An orthotopic model was used to explore microglial infiltration, tumor growth, and invasion into the brain parenchyma. Cell proliferation, migration, invasion, proteome remodeling, and secretome were assayed in vitro. Conditioned media were used to assay angiogenesis, monocyte chemoattraction, and differentiation into macrophages in vitro.CoQCoQ
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- 2022
7. Ubiquinol Supplementation Improves Gender-Dependent Cerebral Vasoreactivity and Ameliorates Chronic Inflammation and Endothelial Dysfunction in Patients with Mild Cognitive Impairment
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Mario Durán-Prado, Javier Domínguez-Bértalo, Francisco J. Alcaín, Cristina M. Pedrero-Prieto, Eloy García-Pérez, Julia Vaamonde, Javier Frontiñán-Rubio, Sonia García-Carpintero, and Mariano Amo-Salas
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Ubiquinol ,medicine.medical_specialty ,LPS ,Physiology ,Clinical Biochemistry ,Inflammation ,macromolecular substances ,030204 cardiovascular system & hematology ,Placebo ,Biochemistry ,Gastroenterology ,Article ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,mild cognitive impairment ,Internal medicine ,coenzyme Q10 ,Medicine ,Dementia ,Viability assay ,Endothelial dysfunction ,Molecular Biology ,Coenzyme Q10 ,business.industry ,lcsh:RM1-950 ,Cell Biology ,medicine.disease ,Endothelial stem cell ,lcsh:Therapeutics. Pharmacology ,chemistry ,breath holding index ,endothelial necrosis ,medicine.symptom ,business ,030217 neurology & neurosurgery - Abstract
Ubiquinol can protect endothelial cells from multiple mechanisms that cause endothelial damage and vascular dysfunction, thus contributing to dementia. A total of 69 participants diagnosed with mild cognitive impairment (MCI) received either 200 mg/day ubiquinol (Ub) or placebo for 1 year. Cognitive assessment of patients was performed at baseline and after 1 year of follow-up. Patients&rsquo, cerebral vasoreactivity was examined using transcranial Doppler sonography, and levels of Ub and lipopolysaccharide (LPS) in plasma samples were quantified. Cell viability and necrotic cell death were determined using the microvascular endothelial cell line bEnd3. Coenzyme Q10 (CoQ) levels increased in patients supplemented for 1 year with ubiquinol versus baseline and the placebo group, although higher levels were observed in male patients. The higher cCoQ concentration in male patients improved cerebral vasoreactivity CRV and reduced inflammation, although the effect of Ub supplementation on neurological improvement was negligible in this study. Furthermore, plasma from Ub-supplemented patients improved the viability of endothelial cells, although only in T2DM and hypertensive patients. This suggests that ubiquinol supplementation could be recommended to reach a concentration of 5 &mu, g/mL in plasma in MCI patients as a complement to conventional treatment.
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- 2021
8. A comprehensive systematic review of CSF proteins and peptides that defne Alzheimer’s disease
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Cristina Aguilera García, Juan R. Peinado, Sonia García-Carpintero, Francisco J. Alcaín, Cristina M. Pedrero-Prieto, Iris Lindberg, Javier Frontiñán-Rubio, Emilio Llanos-González, Mario Durán-Prado, and Yoana Rabanal-Ruiz
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0301 basic medicine ,Clinical Biochemistry ,Peptide ,Disease ,Computational biology ,Review ,Biology ,Proteomics ,03 medical and health sciences ,0302 clinical medicine ,Direct analysis ,Peptidomics ,Molecular Biology ,chemistry.chemical_classification ,Tryptic peptide ,Proteomic ,General Medicine ,Alzheimer´s Disease ,Mass spectrometric ,030104 developmental biology ,chemistry ,Potential biomarkers ,Csf biomarkers ,Molecular Medicine ,030217 neurology & neurosurgery ,Biomarkers - Abstract
Background During the last two decades, over 100 proteomics studies have identified a variety of potential biomarkers in CSF of Alzheimer’s (AD) patients. Although several reviews have proposed specific biomarkers, to date, the statistical relevance of these proteins has not been investigated and no peptidomic analyses have been generated on the basis of specific up- or down- regulation. Herein, we perform an analysis of all unbiased explorative proteomics studies of CSF biomarkers in AD to critically evaluate whether proteins and peptides identified in each study are consistent in distribution; direction change; and significance, which would strengthen their potential use in studies of AD pathology and progression. Methods We generated a database containing all CSF proteins whose levels are known to be significantly altered in human AD from 47 independent, validated, proteomics studies. Using this database, which contains 2022 AD and 2562 control human samples, we examined whether each protein is consistently present on the basis of reliable statistical studies; and if so, whether it is over- or under-represented in AD. Additionally, we performed a direct analysis of available mass spectrometric data of these proteins to generate an AD CSF peptide database with 3221 peptides for further analysis. Results Of the 162 proteins that were identified in 2 or more studies, we investigated their enrichment or depletion in AD CSF. This allowed us to identify 23 proteins which were increased and 50 proteins which were decreased in AD, some of which have never been revealed as consistent AD biomarkers (i.e. SPRC or MUC18). Regarding the analysis of the tryptic peptide database, we identified 87 peptides corresponding to 13 proteins as the most highly consistently altered peptides in AD. Analysis of tryptic peptide fingerprinting revealed specific peptides encoded by CH3L1, VGF, SCG2, PCSK1N, FBLN3 and APOC2 with the highest probability of detection in AD. Conclusions Our study reveals a panel of 27 proteins and 21 peptides highly altered in AD with consistent statistical significance; this panel constitutes a potent tool for the classification and diagnosis of AD.
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- 2020
9. Influence of gender and menopausal status on gut microbiota
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María M. Malagón, Oriol A. Rangel-Zuñiga, Antonio Camargo, Jose Lopez-Miranda, Gracia M. Quintana-Navarro, Rosa Jimenez-Lucena, Manuel Tena-Sempere, Jose A. Santos-Marcos, Blanca B. Landa, Francisco Pérez-Jiménez, Pablo Perez-Martinez, and Sonia García-Carpintero
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Leptin ,Male ,0301 basic medicine ,Physiology ,030209 endocrinology & metabolism ,Gut flora ,General Biochemistry, Genetics and Molecular Biology ,Body Mass Index ,03 medical and health sciences ,0302 clinical medicine ,Glucagon-Like Peptide 1 ,medicine ,Humans ,Chemokine CCL2 ,Sex Characteristics ,biology ,Adiponectin ,Interleukin-6 ,business.industry ,Obstetrics and Gynecology ,Middle Aged ,biology.organism_classification ,medicine.disease ,Obesity ,Gastrointestinal Microbiome ,Sexual dimorphism ,030104 developmental biology ,Female ,Menopause ,Roseburia ,business ,Body mass index ,Hormone - Abstract
Objectives We explore the differences in the gut microbiota associated with gender and hormonal status. Study design We included 76 individuals in this study: 17 pre-menopausal women, 19 men matched by age, as a control group for the pre-menopausal women, 20 post-menopausal women and 20 men matched by age as a control group for the post-menopausal women; all 4 groups were also matched by body mass index (BMI) and nutritional background. Main measurements We analyzed the differences in the gut microbiota, endotoxemia, intestinal incretins, pro-inflammatory cytokines, and plasma levels of energy homeostasis regulatory hormones between pre- and post-menopausal women and compared them with their respective male control groups. Results We found a higher Firmicutes/Bacteroidetes ratio, a higher relative abundance of Lachnospira and Roseburia, and higher GLP-1 plasma levels in pre-menopausal women than in post-menopausal women, who had similar levels to men. In contrast, we observed a lower relative abundance of the Prevotella, Parabacteroides and Bilophila genera, and IL-6 and MCP-1 plasma levels in pre-menopausal women than in post-menopausal women, who had similar levels to the men. We also found higher GiP and leptin plasma levels in women than in men, irrespective of the menopausal status of the women. In addition, adiponectin levels were higher in pre-menopausal women than in their corresponding age-matched male control group. Conclusions Our results suggest that the differences in the composition of gut microbiota between genders and between women of different hormonal status may be related to the sexual dimorphism observed in the incidence of metabolic diseases and their co-morbidities.
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- 2018
10. The gut microbial community in metabolic syndrome patients is modified by diet
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Francisco Gomez-Delgado, Juan F. Alcala-Diaz, Jose Lopez-Miranda, Antonio Camargo, Blanca B. Landa, Carmen Haro, Oriol A. Rangel Zuñiga, Jose C. Clemente, Sonia García-Carpintero, Gracia M. Quintana-Navarro, Francisco Pérez-Jiménez, Pablo Perez-Martinez, Javier Delgado-Lista, Fundación Patrimonio Comunal Olivarero, Junta de Andalucía, Diputación de Jaén, Diputación de Córdoba, Ministerio de Medio Ambiente y Medio Rural y Marino (España), Ministerio de Ciencia e Innovación (España), Ministerio de Economía y Competitividad (España), European Commission, and Instituto de Salud Carlos III
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0301 basic medicine ,Bifidobacterium longum ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Population ,Faecalibacterium prausnitzii ,Gut flora ,Diet, Mediterranean ,medicine.disease_cause ,digestive system ,Biochemistry ,Microbiology ,03 medical and health sciences ,fluids and secretions ,Mediterranean diet ,medicine ,Humans ,Eubacterium ,Obesity ,education ,Molecular Biology ,Metabolic Syndrome ,education.field_of_study ,Nutrition and Dietetics ,Bacteria ,biology ,Microbiota ,food and beverages ,Cardiovascular disease ,biology.organism_classification ,Metabolic syndrome ,Intestines ,030104 developmental biology ,Parabacteroides distasonis ,Bacteroides ,Bacteroides thetaiotaomicron - Abstract
Haro, Carmen et al., Intestinal microbiota changes may be involved in the development of metabolic syndrome (MetS), which is a multicomponent disorder frequently associated with obesity. The aim of this study was to test the effect of consuming two healthy diets: a Mediterranean diet and a low-fat high-carbohydrate diet, for 2 years in the gut microbiota of MetS patients and those in the control group. We analyzed the differences in the bacterial community structure between the groups after 2 years of dietary intervention (Mediterranean or low-fat diet) through quantitative polymerase chain reaction using primers, targeting specific bacterial taxa. We observed, at basal time, that the abundance of Bacteroides, Eubacterium and Lactobacillus genera is lower in the control group than in MetS patients, while Bacteroides fragilis group, Parabacteroides distasonis, Bacteroides thetaiotaomicron, Faecalibacterium prausnitzii, Fusobacterium nucleatum, Bifidobacterium longum, Bifidobacterium adolescentis, Ruminococcus flavefaciens subgroup and Eubacterium rectale are depleted in MetS patients (all P values, The CORDIOPREV study is supported by the Fundación Patrimonio Comunal Olivarero, Junta de Andalucía (Consejería de Salud, Consejería de Agricultura y Pesca, Consejería de Innovación and Ciencia y Empresa), Diputaciones de Jaén y Córdoba, Centro de Excelencia en Investigación sobre Aceite de Oliva y Salud and Ministerio de Medio Ambiente, Medio Rural y Marino and Gobierno de España. In addition, it was partly supported by research grants from the Ministerio de Ciencia e Innovación (AGL2009-122270 to J.L.-M., FIS PI10/01041 to P.P.-M. and PI10/02412 to F.P.-J.); Ministerio de Economia y Competitividad (AGL2012/39615 to J.L.-M.); Consejería de Economía, Innovación y Ciencia, Proyectos de Investigación de Excelencia, Junta de Andalucía (AGR922 to F.P.-J.); Consejería de Salud, Junta de Andalucía (PI0193/09 to J.L.-M., 0118/08 to F.F.-J., PI-0252/09 to J.D.-L. and PI-0058/10 to P.P.-M.); Consejería de Innovación Ciencia y Empresa (CVI-7450 to J.L.-M.); and Fondo Europeo de Desarrollo Regional. Antonio Camargo is supported by an Instituto de Salud Carlos III research contract (Programa Miguel-Servet CP14/00114). Carmen Haro is supported by an Instituto de Salud Carlos III research fellow/contract (Programa PFIS F111/00394).
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- 2016
11. Postprandial endotoxemia may influence the development of type 2 diabetes mellitus: From the CORDIOPREV study
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Oriol A. Rangel-Zuñiga, Jose M. Ordovas, Ben van Ommen, Francisco Pérez-Jiménez, Sonia García-Carpintero, Javier Lopez-Moreno, Pablo Perez-Martinez, Rosa Jimenez-Lucena, María M. Malagón, Ruth Blanco-Rojo, Javier Delgado-Lista, Antonio Camargo, Jose Lopez-Miranda, and Juan F. Alcala-Diaz
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0301 basic medicine ,Male ,medicine.medical_specialty ,endocrine system diseases ,030209 endocrinology & metabolism ,Inflammation ,Hyperlipidemias ,Critical Care and Intensive Care Medicine ,Gastroenterology ,Intestinal absorption ,03 medical and health sciences ,0302 clinical medicine ,Insulin resistance ,Internal medicine ,Diabetes mellitus ,medicine ,Humans ,Receptor ,030109 nutrition & dietetics ,Nutrition and Dietetics ,business.industry ,nutritional and metabolic diseases ,Type 2 Diabetes Mellitus ,Middle Aged ,medicine.disease ,Postprandial Period ,Endotoxemia ,Postprandial ,Diabetes Mellitus, Type 2 ,Biomarker (medicine) ,Female ,medicine.symptom ,Insulin Resistance ,business - Abstract
Insulin resistance (IR) and impaired beta-cell function are key determinants of type 2 diabetes mellitus (T2DM). Intestinal absorption of bacterial components activates the toll-like receptors inducing inflammation, and this in turn IR. We evaluated the role of endotoxemia in promoting inflammation-induced insulin resistance (IR) in the development of T2DM, and its usefulness as predictive biomarker.We included in this study 462 patients from the CORDIOPREV study without T2DM at baseline. Of these, 107 patients developed T2DM according to the American Diabetes Association (ADA) diagnosis criteria after a median follow-up of 60 months (Incident-DIAB group), whereas 355 patients did not developed it during this period of time (Non-DIAB group).We observed a postprandial increase in lipopolysaccharides (LPS) levels in the Incident-DIAB at baseline (P 0.001), whereas LPS levels were not modified in the Non-DIAB. Disease-free survival curves based on the LPS postprandial fold change improved T2DM Risk Assessment as compared with the previously described FINDRISC score (hazard ratio of 2.076, 95% CI 1.149-3.750 vs. 1.384, 95% CI 0.740-2.589). Moreover, disease-free survival curves combining the LPS postprandial fold change and FINDRISC score together showed a hazard ratio of 3.835 (95% CI 1.323-11.114), linked to high values of both parameters.Our results suggest that a high postprandial endotoxemia precedes the development of T2DM. Our results also showed the potential use of LPS plasma levels as a biomarker predictor of T2DM development. CLINICAL TRIALS.GOV.NCT00924937.
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- 2017
12. Endotoxemia is modulated by quantity and quality of dietary fat in older adults
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Oriol A. Rangel-Zuñiga, Elena M. Yubero-Serrano, Sonia García-Carpintero, Pablo Perez-Martinez, Irene Roncero-Ramos, Rosa Jimenez-Lucena, Juan F. Alcala-Diaz, Antonio Camargo, Francisco Gomez-Delgado, María M. Malagón, Jose M. Ordovas, Javier Lopez-Moreno, Cristina Vals-Delgado, and Jose Lopez-Miranda
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0301 basic medicine ,Lipopolysaccharides ,Male ,Aging ,medicine.medical_specialty ,Mediterranean diet ,Population ,Inflammation ,Biology ,Diet, Mediterranean ,Biochemistry ,03 medical and health sciences ,Endocrinology ,Internal medicine ,Genetics ,medicine ,Ingestion ,Humans ,education ,Molecular Biology ,Aged ,chemistry.chemical_classification ,Meal ,education.field_of_study ,Cross-Over Studies ,Membrane Glycoproteins ,food and beverages ,Cell Biology ,Middle Aged ,Atherosclerosis ,Crossover study ,Dietary Fats ,Endotoxemia ,030104 developmental biology ,Postprandial ,chemistry ,lipids (amino acids, peptides, and proteins) ,Female ,medicine.symptom ,Carrier Proteins ,Polyunsaturated fatty acid ,Acute-Phase Proteins - Abstract
Background Aging is an important determinant of the rate of atherosclerosis development, mainly through low-grade inflammation. Diet, and particularly its fat content, modulates the inflammatory response in fasting and postprandial states. Objective We aimed to study the effects of dietary fat on endotoxemia in healthy older adults. Materials and methods Twenty healthy older adults were randomized to three diets, lasting three-weeks each, using a crossover design: 1. A Mediterranean diet enriched in MUFA with virgin olive oil. 2. An SFA-rich diet. 3. A low-fat high-carbohydrate diet enriched in n-3 PUFA (α-linolenic acid of plant origin) (CHO-PUFA diet). At the end of each period, after a 12-h fast, the subjects received a meal with a composition similar to the dietary period just completed. We determined the fasting and the postprandial plasma levels of lipopolysaccharide (LPS) and LPS-binding protein (LBP). Results In the fasting state, we observed lower LPS plasma levels after the consumption of the CHO-PUFA diet ( P = 0.046) in comparison with the consumption of the Med and SFA-rich diets. In the postprandial measurements, we observed a statistically significant increase in plasma levels of LPS ( P = 0.044) and a decrease in LBP ( P = 0.003) after the intake of the CHO-PUFA meal, whereas no postprandial changes were observed after the ingestion of the Med and SFA-rich meals. Conclusion Our results, together with those obtained in a previous study, support the concept that the consumption of the Med Diet, in contrast to a low-fat PUFA diet, constitutes a more suitable dietary lifestyle for preventing the development of atherosclerosis in a population at risk, such as older adults.
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- 2017
13. Effect of Dietary Lipids on Endotoxemia Influences Postprandial Inflammatory Response
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Sonia García-Carpintero, Rosa Jimenez-Lucena, Javier Lopez-Moreno, Pablo Perez-Martinez, Carmen Haro, Helen M. Roche, Francisco J. Tinahones, Elena M. Yubero-Serrano, Jose Lopez-Miranda, Javier Delgado-Lista, Antonio Camargo, Ruth Blanco-Rojo, and Oriol A. Rangel-Zuñiga
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0301 basic medicine ,Male ,medicine.medical_specialty ,Saturated fat ,Adipose tissue ,030209 endocrinology & metabolism ,Inflammation ,Biology ,medicine.disease_cause ,Peripheral blood mononuclear cell ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,medicine ,Humans ,chemistry.chemical_classification ,Metabolic Syndrome ,General Chemistry ,Middle Aged ,medicine.disease ,Postprandial Period ,Dietary Fats ,Endotoxemia ,MSH Release-Inhibiting Hormone ,Oxidative Stress ,030104 developmental biology ,Postprandial ,Endocrinology ,chemistry ,Leukocytes, Mononuclear ,Female ,medicine.symptom ,Metabolic syndrome ,General Agricultural and Biological Sciences ,Oxidative stress ,Polyunsaturated fatty acid - Abstract
Metabolic syndrome (MetS) results in postprandial metabolic alterations that predisposes one to a state of chronic low-grade inflammation and increased oxidative stress. We aimed to assess the effect of the consumption of the quantity and quality of dietary fat on fasting and postprandial plasma lipopolysaccharides (LPS). A subgroup of 75 subjects with metabolic syndrome was randomized to receive 1 of 4 diets: HSFA, rich in saturated fat; HMUFA, rich in monounsaturated fat; LFHCC n-3, low-fat, rich in complex carbohydrate diet supplemented with n-3 polyunsaturated fatty acids; LFHCC low-fat, rich in complex carbohydrate diet supplemented with placebo, for 12 weeks each. We administered a fat challenge reflecting the fatty acid composition of the diets at postintervention. We determined the plasma lipoproteins and glucose and gene expression in peripheral blood mononuclear cells (PBMC) and adipose tissue. LPS and LPS binding protein (LBP) plasma levels were determined by ELISA, at fasting and postprandial (4 h after a fat challenge) states. We observed a postprandial increase in LPS levels after the intake of the HSFA meal, whereas we did not find any postprandial changes after the intake of the other three diets. Moreover, we found a positive relationship between the LPS plasma levels and the gene expression of IkBa and MIF1 in PBMC. No statistically significant differences in the LBP plasma levels at fasting or postprandial states were observed. Our results suggest that the consumption of HSFA diet increases the intestinal absorption of LPS which, in turn, increases postprandial endotoxemia levels and the postprandial inflammatory response.
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- 2017
14. Consumption of Two Healthy Dietary Patterns Restored Microbiota Dysbiosis in Obese Patients with Metabolic Dysfunction
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Oriol A. Rangel-Zuñiga, Francisco Pérez-Jiménez, Jose Lopez-Miranda, Blanca B. Landa, Pablo Perez-Martinez, Antonio Camargo, Juan F. Alcala-Diaz, Carmen Haro, Jose C. Clemente, Sonia García-Carpintero, Fundación Patrimonio Comunal Olivarero, Junta de Andalucía, Diputación de Córdoba, Diputación de Jaén, Ministerio de Medio Ambiente y Medio Rural y Marino (España), Instituto de Salud Carlos III, Ministerio de Economía y Competitividad (España), and European Commission
- Subjects
Male ,0301 basic medicine ,medicine.medical_specialty ,Calorie ,Saturated fat ,Physiology ,Biology ,Diet, Mediterranean ,Feces ,03 medical and health sciences ,Internal medicine ,medicine ,Humans ,Obesity ,Diet, Fat-Restricted ,Metabolic Syndrome ,chemistry.chemical_classification ,Middle Aged ,medicine.disease ,Coronary heart disease ,Gut microbiome ,Gastrointestinal Microbiome ,Treatment Outcome ,030104 developmental biology ,Endocrinology ,chemistry ,Dysbiosis ,Metabolic syndrome ,Food Science ,Biotechnology ,Polyunsaturated fatty acid - Abstract
[Scope] The consumption of two healthy diets (Mediterranean (MED) and low‐fat (LF) diets) may restore the gut microbiome dysbiosis in obese patients depending on the degree of metabolic dysfunction., [Methods and results] The differences in bacterial community at baseline and after 2 years of dietary intervention of 106 subjects from the CORDIOPREV study were analyzed, 33 of whom were obese patients with severe metabolic disease (5 criteria for metabolic syndrome) (MetS‐OB), 32 obese patients without metabolic dysfunction (2 or less criteria for metabolic syndrome) (NonMetS‐OB) and 41 non‐obese subjects (NonMetS‐NonOB). Our study showed a marked dysbiosis in people with severe metabolic disease (Met‐OB), compared with obese people without MetS (NonMetS‐OB) and non‐obese people (NonMetS‐NonOB). This disbiotic pattern was reversed by consumption of both MED (35% of calories as fat (22% MUFA fat, 6% PUFA fat and, [Conclusion] Our results suggest that the chronic intake of two healthy dietary patterns partially restores the gut microbiome dysbiosis in obese patients with coronary heart disease, depending on the degree of metabolic dysfunction., The CORDIOPREV study is supported by the Fundación Patrimonio Comunal Olivarero, Junta de Andalucía (Consejería de Salud, Consejería de Agricultura y Pesca, Consejería de Innovación, Ciencia y Empresa), Diputaciones de Jaén y Córdoba, Centro de Excelencia en Investigación sobre Aceite de Oliva y Salud and Ministerio de Medio Ambiente, Medio Rural y Marino, Gobierno de España. The CIBEROBN is an initiative of the Instituto de Salud Carlos III, Madrid, Spain. It was also partly supported by research grants from Ministerio de Economía y Competitividad (AGL2012/39615, PIE14/00005, and PIE 14/00031 to J.L.‐M.; AGL2015/‐67896‐P to J.L.‐M. and A.C.; CP14/00114 to A.C.; FIS PI13/00023 to J.D.‐L.; FIS PI13/00185 to P. P.‐M.; PI13/00619 to F. P.‐J.; FIS PI16/01777 to P. P.‐M. and F. P.‐J.); Consejería de Innovación, Ciencia y Empresa, Proyectos de Investigación de Excelencia, Junta de Andalucía (CVI‐7450 to J. L.‐M.); Fondo Europeo de Desarrollo Regional (FEDER). A. C. is supported by an ISCIII research contract, Instituto de Salud Carlos III (Programa Miguel‐Servet CP14/00114).
- Published
- 2017
15. Postprandial endotoxemia may influence the type 2 diabetes mellitus development
- Author
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Sonia García-Carpintero, Javier Lopez-Moreno, Pablo Perez-Martinez, Antonio Camargo Garcia, Rosa Jimenez-Lucena, Jose D Torres-Peña, Elena M. Yubero-Serrano, Ana Leon-Acuña, Oriol A. Rangel-Zuñiga, and Jose Lopez-Miranda
- Subjects
medicine.medical_specialty ,Endocrinology ,Postprandial ,business.industry ,Internal medicine ,medicine ,Type 2 Diabetes Mellitus ,Cardiology and Cardiovascular Medicine ,business - Published
- 2017
16. Interaction between genetic polymorphism at the gckr gene and smoking status influences intima media thickness: From the cordioprev study
- Author
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Pablo Perez-Martinez, J. Criado-Garcia, Ana I. Perez-Caballero, J. Delgado Lista, Sonia García-Carpintero, Francisco Gomez-Delgado, and Antonio Garcia-Rios
- Subjects
medicine.medical_specialty ,Endocrinology ,Intima-media thickness ,Internal medicine ,medicine ,Smoking status ,Biology ,Cardiology and Cardiovascular Medicine ,Gene - Published
- 2014
17. Dietary fat may modulate adipose tissue homeostasis through the processes of autophagy and apoptosis
- Author
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Francisco Gomez-Delgado, Francisco J. Tinahones, Jose Lopez-Miranda, Yolanda Almaden, Javier Lopez-Moreno, Pablo Perez-Martinez, Javier Delgado-Lista, Sonia García-Carpintero, Helen M. Roche, Oriol A. Rangel-Zuñiga, Juan F. Alcala-Diaz, Carmen Marin, Antonio Camargo, and Elena M. Yubero-Serrano
- Subjects
0301 basic medicine ,Blood Glucose ,Male ,Medicine (miscellaneous) ,Adipose tissue ,Apoptosis ,Autophagy-Related Protein 7 ,Fatty Acids, Monounsaturated ,0302 clinical medicine ,Adipocytes ,Homeostasis ,Single-Blind Method ,Diet, Fat-Restricted ,chemistry.chemical_classification ,Caspase 7 ,Metabolic Syndrome ,Nutrition and Dietetics ,Caspase 3 ,Fatty Acids ,BECN1 ,Middle Aged ,Adipose Tissue ,030220 oncology & carcinogenesis ,Beclin-1 ,Female ,Polyunsaturated fatty acid ,Adult ,medicine.medical_specialty ,Biology ,Diet, High-Fat ,03 medical and health sciences ,Insulin resistance ,Internal medicine ,Fatty Acids, Omega-3 ,medicine ,Autophagy ,Humans ,Obesity ,Aged ,Fatty acid ,medicine.disease ,Dietary Fats ,030104 developmental biology ,Endocrinology ,chemistry ,Gene Expression Regulation ,Metabolic syndrome ,Insulin Resistance - Abstract
Obesity increases the risk of cardiovascular disease, type 2 diabetes mellitus and cancer development. Autophagy and apoptosis are critical processes for development and homeostasis in multicellular organisms and have been linked to a variety of disorders. We aimed to investigate whether the quantity and quality of dietary fat can influence these processes in the adipose tissue of obese people. A randomized, controlled trial within the LIPGENE study assigned 39 obese people with metabolic syndrome to 1 of 4 diets: (a) a high-saturated fatty acid diet, (b) a high-monounsaturated fatty acid (HMUFA) diet, and (c, d) two low-fat, high-complex carbohydrate diets supplemented with long-chain n-3 polyunsaturated fatty acids (LFHCC n-3) or placebo (LFHCC), for 12 weeks each. We found an increase in the expression of autophagy-related BECN1 and ATG7 genes after the long-term consumption of the HMUFA diet (p = 0.001 and p = 0.004, respectively) and an increase in the expression of the apoptosis-related CASP3 gene after the long-term consumption of the LFHCC and LFHCC n-3 diets (p = 0.001 and p = 0.029, respectively). CASP3 and CASP7 gene expression changes correlated with HOMA index. Our results suggest that the processes of autophagy and apoptosis in adipose tissue may be modified by diet and that the consumption of a diet rich in monounsaturated fat may contribute to adipose tissue homeostasis by increasing autophagy. They also reinforce the notion that apoptosis in adipose tissue is linked to insulin resistance. ClinicalTrials.gov NCT00429195.
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