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Your search keyword '"García Fuentes, E"' showing total 209 results
Start Over Author "García Fuentes, E" Publication Type Academic Journals
209 results on '"García Fuentes, E"'

5. Iodine intake in the adult population. Di@bet.es study

Author

Soriguer, F., García-Fuentes, E., Gutierrez-Repiso, C., Rojo-Martínez, G., Velasco, I., Goday, A., Bosch-Comas, A., Bordiú, E., Calle, A., Carmena, R., Casamitjana, R., Castaño, L., Castell, C., Catalá, M., Delgado, E., Franch, J., Gaztambide, S., Girbés, J., Gomis, R., Gutiérrez, G., López-Alba, A., Martínez-Larrad, M.T., Menéndez, E., Mora-Peces, I., Ortega, E., Pascual-Manich, G., Serrano-Rios, M., Valdés, S., Vázquez, J.A., and Vendrell, J.

Published
2012
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30. Resistin Regulates Pituitary Lipid Metabolism and Inflammation In Vivo and In Vitro.

Author

Rodriguez-Pacheco, F., Novelle, M. G., Vazquez, M. J., Garcia-Escobar, E., Soriguer, F., Rojo-Martinez, G., García-Fuentes, E., Malagon, M. M., and Dieguez, C.

Subjects
RESISTIN, ADIPOKINES, LIPID metabolism, INFLAMMATION, MESSENGER RNA, LABORATORY rats, IN vitro studies
Abstract

The adipokine resistin is an insulin-antagonizing factor that also plays a regulatory role in inflammation, immunity, food intake, and gonadal function and also regulates growth hormone (GH) secretion in rat adenopituitary cells cultures with the adipokine. Although adipose tissue is the primary source of resistin, it is also expressed in other tissues, including the pituitary. The aim of this study is to investigate the possible action of resistin on the lipid metabolism in the pituitary gland in vivo (rats in two different nutritional status, fed and fast, treated with resistin on acute and a chronic way) and in vitro (adenopituitary cell cultures treated with the adipokine).Here, by a combination of in vivo and in vitro experimental models, we demonstrated that central acute and chronic administration of resistin enhance mRNA levels of the lipid metabolic enzymes which participated on lipolysis and moreover inhibiting mRNA levels of the lipid metabolic enzymes involved in lipogenesis. Taken together, our results demonstrate for the first time that resistin has a regulatory role on lipid metabolism in the pituitary gland providing a novel insight in relation to the mechanism by which this adipokine can participate in the integrated control of lipid metabolism. [ABSTRACT FROM AUTHOR]

Published
2013
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48. Weight Loss After Sleeve Gastrectomy According to Metabolic Dysfunction-Associated Steatotic Liver Disease Stage in Patients with Obesity: A Liver Biopsy-Based Prospective Study.

Author

Martínez-Montoro JI, Arranz-Salas I, Gutiérrez-Repiso C, Sánchez-García A, Ocaña-Wilhelmi L, Pinazo-Bandera JM, Fernández-García D, Muñoz-Garach A, Morales-García D, García-Cortés M, García-Fuentes E, Tinahones FJ, and Garrido-Sánchez L

Subjects
Humans, Female, Male, Prospective Studies, Adult, Biopsy, Middle Aged, Obesity, Morbid surgery, Obesity, Morbid complications, Bariatric Surgery, Weight Loss, Gastrectomy methods, Gastrectomy adverse effects, Liver pathology, Fatty Liver etiology, Obesity complications, Obesity surgery
Abstract

Background: The role of metabolic dysfunction-associated steatotic liver disease (MASLD) in sleeve gastrectomy (SG)-related outcomes remains uncertain. In this study, we aimed to assess the influence of preoperative biopsy-proven MASLD and its stages on weight loss after SG., Methods: One hundred sixty-three patients with obesity undergoing SG with concomitant intraoperative liver biopsy were followed up for 1 year. Fifty-eight participants were categorized as no MASLD, thirty-eight as metabolic dysfunction-associated steatotic liver (MASL), and sixty-seven as metabolic dysfunction-associated steatohepatitis (MASH). Percentage total weight loss (%TWL) and percentage excess weight loss (%EWL) 1 year after SG were calculated for the different groups. We also evaluated the association between preoperative MASLD (and its stages) and weight loss, after adjusting for potential confounders., Results: Significant differences among groups were detected in %EWL ( p = 0.004, ANOVA test), but not in %TWL ( p = 0.079). However, significant differences in %TWL were found when MASH and no MASH (i.e., participants with MASL and participants without MASLD) groups were compared (27.3 ± 9.9 vs. 30.7 ± 9, respectively, p = 0.025). In the linear regression model for predicting %EWL 1 year after SG, the presence of MASH was independently associated with a lower %EWL, after adjusting for age, sex, baseline body mass index (BMI), and baseline glycated hemoglobin (HbA1c) (Beta -7.1; 95% CI -13.6, -0.5; p = 0.035). The presence of MASLD, liver fibrosis, or advanced liver fibrosis (≥F2) was also associated with lower %EWL after SG in crude models, although they did not remain significant after adjusting for these confounders. The presence of MASH was inversely related to %TWL, although the association did not remain significant after adjustment (Beta -2.7; 95% CI -5.7, 0.2; p = 0.069)., Conclusions: MASH may be independently associated with lower %EWL 1 year after SG in patients with obesity.

Published
2024
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49. The Expression of Genes Related to Reverse Cholesterol Transport and Leptin Receptor Pathways in Peripheral Blood Mononuclear Cells Are Decreased in Morbid Obesity and Related to Liver Function.

Author

Jiménez-Cortegana C, López-Enríquez S, Alba G, Santa-María C, Martín-Núñez GM, Moreno-Ruiz FJ, Valdés S, García-Serrano S, Rodríguez-Díaz C, Ho-Plágaro A, Fontalba-Romero MI, García-Fuentes E, Garrido-Sánchez L, and Sánchez-Margalet V

Subjects
Humans, Male, Female, Adult, Middle Aged, ATP Binding Cassette Transporter, Subfamily G, Member 1 metabolism, ATP Binding Cassette Transporter, Subfamily G, Member 1 genetics, Signal Transduction, Biological Transport, Gene Expression Regulation, Non-alcoholic Fatty Liver Disease metabolism, Non-alcoholic Fatty Liver Disease genetics, Adaptor Proteins, Signal Transducing metabolism, Adaptor Proteins, Signal Transducing genetics, Obesity, Morbid metabolism, Obesity, Morbid surgery, Obesity, Morbid genetics, Leukocytes, Mononuclear metabolism, Receptors, Leptin genetics, Receptors, Leptin metabolism, Cholesterol metabolism, Liver X Receptors metabolism, Liver X Receptors genetics, ATP Binding Cassette Transporter 1 genetics, ATP Binding Cassette Transporter 1 metabolism, Liver metabolism
Abstract

Obesity is frequently accompanied by non-alcoholic fatty liver disease (NAFLD). These two diseases are associated with altered lipid metabolism, in which reverse cholesterol transport (LXRα/ABCA1/ABCG1) and leptin response (leptin receptor (Ob-Rb)/Sam68) are involved. The two pathways were evaluated in peripheral blood mononuclear cells (PBMCs) from 86 patients with morbid obesity (MO) before and six months after Roux-en-Y gastric bypass (RYGB) and 38 non-obese subjects. In the LXRα pathway, LXRα, ABCA1, and ABCG1 mRNA expressions were decreased in MO compared to non-obese subjects ( p < 0.001, respectively). Ob-Rb was decreased ( p < 0.001), whereas Sam68 was increased ( p < 0.001) in MO. RYGB did not change mRNA gene expressions. In the MO group, the LXRα pathway (LXRα/ABCA1/ABCG1) negatively correlated with obesity-related variables (weight, body mass index, and hip), inflammation (C-reactive protein), and liver function (alanine-aminotransferase, alkaline phosphatase, and fatty liver index), and positively with serum albumin. In the Ob-R pathway, Ob-Rb and Sam68 negatively correlated with alanine-aminotransferase and positively with albumin. The alteration of LXRα and Ob-R pathways may play an important role in NAFLD development in MO. It is possible that MO patients may require more than 6 months following RYBGB to normalize gene expression related to reverse cholesterol transport or leptin responsiveness.

Published
2024
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50. Mitochondrial Stress Links Environmental Triggers with Pro-Inflammatory Signaling in Crohn's Disease.

Author

Martín-Reyes F, Bernal M, Rodríguez-Díaz C, Rodríguez-de Los Reyes D, Ho-Plagaro A, Rodríguez-Pacheco F, Camacho-Martel L, Camargo-Camero R, Rodríguez-González FJ, Alcain-Martínez G, Martín-Masot R, Navas-López VM, Villanueva-Paz M, Lucena MI, García-Fuentes E, and López-Gómez C

Abstract

Inflammatory Bowel Diseases (IBD) are a group of chronic, inflammatory disorders of the gut. The incidence and activity of IBD are determined by both genetic and environmental factors. Among these factors, polymorphisms in genes related to autophagy and the consumption of non-steroidal anti-inflammatory drugs (NSAIDs) have been consistently associated with IBD. We show that NSAIDs induce mitochondrial stress and mitophagy in intestinal epithelial cells. In an altered mitophagy context simulating that observed in IBD patients, NSAID-induced mitochondrial stress leads to the release of mitochondrial components, which act as Danger Associated Molecular Patterns with pro-inflammatory potential. Furthermore, colonic organoids from Crohn's disease patients and healthy donors show activation of the mitochondrial Unfolded Protein Response (UPR mt ) upon treatment with ibuprofen. Finally, colon biopsies from Crohn's disease patients in remission or with low-to-moderate activity also show expression of genes involved in UPR mt , while patients with severe activity show no increase compared to healthy donors. Our results suggest the involvement of mitochondria in the mechanisms triggering inflammation in IBD after NSAID use. Moreover, our results highlight the clinical relevance of mitochondrial stress and activation of the UPR mt pathway in the pathophysiology of Crohn's disease.

Published
2023
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