Browsing by Keyword "Glucose"
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Publication Fasentin diminishes endothelial cell proliferation, differentiation and invasion in a glucose metabolism-independent manner(Springer, 2020-04-09) Ocaña, M. Carmen; Martínez-Poveda, Beatriz; Marí-Beffa, Manuel; Quesada, Ana R.; Medina, Miguel Ángel; [Ocaña,MC; Martínez-Poveda,B; Quesada,AR; Medina,MÁ] Universidad de Málaga, Andalucía Tech, Departamento de Biología Molecular y Bioquímica, Facultad de Ciencias, Málaga, Spain. [Ocaña,MC; Martínez-Poveda,B; Quesada,AR; Medina,MÁ] IBIMA (Biomedical Research Institute of Málaga), Málaga, Spain. [Marí-Beffa,M] Universidad de Málaga, Andalucía Tech, Departamento de Biología Celular, Genética y Fisiología, Facultad de Ciencias, Málaga, Spain. [Quesada,AR; Medina,MÁ] CIBER de Enfermedades Raras (CIBERER), Málaga, Spain.The synthetic compound fasentin has been described as a modulator of GLUT-1 and GLUT-4 transporters, thus inhibiting glucose uptake in some cancer cells. Endothelial glucose metabolism has been recently connected to angiogenesis and it is now an emerging topic in scientific research. Indeed, certain compounds with a known effect on glucose metabolism have also been shown to inhibit angiogenesis. In this work we tested the capability of fasentin to modulate angiogenesis in vitro and in vivo. We show that fasentin inhibited tube formation in endothelial cells by a mechanism that involves a negative effect on endothelial cell proliferation and invasion, without affecting other steps related to the angiogenic process. However, fasentin barely decreased glucose uptake in human dermal microvascular endothelial cells and the GLUT-1 inhibitor STF-31 failed to inhibit tube formation in these cells. Therefore, this modulatory capacity on endothelial cells function exerted by fasentin is most likely independent of a modulation of glucose metabolism. Taken together, our results show a novel biological activity of fasentin, which could be evaluated for its utility in cancer and other angiogenesis-dependent diseases.Publication Interplay of Glycemic Index, Glycemic Load, and Dietary Antioxidant Capacity with Insulin Resistance in Subjects with a Cardiometabolic Risk Profile(Multidisciplinary Digital Publishing Institute (MDPI), 2018-11) Galarregui, Cristina; Angeles Zulet, Maria; Cantero, Irene; Araceli Marin-Alejandre, Bertha; Ignacio Monreal, Jose; Elorz, Mariana; Benito-Boillos, Alberto; Ignacio Herrero, Jose; Tur, Josep A; Abete, Itziar; Alfredo Martinez, JoseBackground: Dietary total antioxidant capacity (TAC), glycemic index (GI), and glycemic load (GL) are accepted indicators of diet quality, which have an effect on diet-disease relationships. The aim of this study was to evaluate potential associations of dietary TAC, GI, and GL with variables related to nutritive status and insulin resistance (IR) risk in cardiometabolic subjects. Methods: A total of 112 overweight or obese adults (age: 50.8 +/- 9 years old) were included in the trial. Dietary intake was assessed by a validated 137-item food frequency questionnaire (FFQ), which was also used to calculate the dietary TAC, GI, and GL. Anthropometrics, blood pressure, body composition by dual-energy X-ray absorptiometry (DXA), glycemic and lipid profiles, C-reactive protein (CRP), as well as fatty liver quantification by magnetic resonance imaging (MRI) were assessed. Results: Subjects with higher values of TAC had significantly lower circulating insulin concentration and homeostatic model assessment of insulin resistance (HOMA-IR). Participants with higher values of HOMA-IR showed significantly higher GI and GL. Correlation analyses showed relevant inverse associations of GI and GL with TAC. A regression model evidenced a relationship of HOMA-IR with TAC, GI, and GL. Conclusion: This data reinforces the concept that dietary TAC, GI, and GL are potential markers of diet quality, which have an impact on the susceptible population with a cardiometabolic risk profile.Publication Nitric oxide compounds have different effects profiles on human articular chondrocyte metabolism(BioMed Central (BMC), 2013-09-11) de Andrés, María C; Maneiro, Emilia; Martín, Miguel A; Arenas, Joaquín; Blanco, Francisco J; Ministerio de Ciencia e Innovación (España); Instituto de Salud Carlos III; Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)INTRODUCTION: The pathogenesis of osteoarthritis (OA) is characterized by the production of high amounts of nitric oxide (NO), as a consequence of up-regulation of chondrocyte-inducible nitric oxide synthase (iNOS) induced by inflammatory cytokines. NO donors represent a powerful tool for studying the role of NO in the cartilage in vitro. There is no consensus about NO effects on articular cartilage in part because the differences between the NO donors available. The aim of this work is to compare the metabolic profile of traditional and new generation NO donors to see which one points out the osteoarthritic process in the best way. METHODS: Human healthy and OA chondrocytes were isolated from patients undergoing joint replacement surgery, and primary cultured. Cells were stimulated with NO donors (NOC-12 or SNP). NO production was evaluated by the Griess method, and apoptosis was quantified by flow cytometry. Mitochondrial function was evaluated by analysing respiratory chain enzyme complexes, citrate synthase (CS) activities by enzymatic assay, mitochondrial membrane potential (Δψm) by JC-1 using flow cytometry, and ATP levels were measured by luminescence assays. Glucose transport was measured as the uptake of 2-deoxy-[(3)H]glucose (2-[(3)H]DG). Statistical analysis was performed using the Mann-Whitney U test. RESULTS: NOC-12 liberates approximately ten times more NO2- than SNP, but the level of cell death induced was not as profound as that produced by SNP. Normal articular chondrocytes stimulated with NOC-12 had reduced activity from complexes I, III y IV, and the mitochondrial mass was increased in these cells. Deleterious effects on ΔΨm and ATP levels were more profound with SNP, and this NO donor was able to reduce 2-[(3)H]DG levels. Both NO donors had opposite effects on lactate release, SNP diminished the levels and NOC-12 lead to lactate accumulation. OA chondrocytes incorporate significantly more 2-[(3)H]DG than healthy cells. CONCLUSIONS: These findings suggest that the new generation donors, specifically NOC-12, mimic the OA metabolic process much better than SNP. Previous results using SNP have to be considered prudently since most of the effects observed can be induced by the interactions of secondary products of NO.Publication Simple sugar intake and cancer incidence, cancer mortality and all- cause mortality: A cohort study from the PREDIMED trial(Churchill Livingstone, 2021-10) Laguna, Juan C; Alegret, Marta; Cofan, Montserrat; Sanchez-Tainta, Ana; Diaz-Lopez, Andres; Martinez-Gonzalez, Miguel A; V. Sorli, Jose; Salas-Salvado, Jordi; Fito, Montserrat; Alonso-Gomez, Angel M; Serra-Majem, Lluis; Laperra, Jose; Fiol Sala, Miquel; Gomez-Gracia, Enrique; Pinto, Xavier; Muñoz, Miguel A; Castaner, Olga; Ramirez-Sabio, Judith B; Portu, Jose J; Estruch, Ramon; Ros, EmilioObjective: To examine associations between intake of simple sugars and cancer incidence, cancer mor-tality, and total mortality in a prospective cohort study based on the PREDIMED trial conducted from 2003 to 2010. Methods: Participants were older individuals at high cardiovascular risk. Exposures were total sugar, glucose and fructose from solid or liquid sources, and fructose from fruit and 100% fruit juice. Cancer incidence was the primary outcome; cancer mortality and all-cause mortality were secondary outcomes. Multivariable-adjusted, time-dependent Cox proportional hazard models were used. Results: of 7447 individuals enrolled, 7056 (94.7%) were included (57.6% women, aged 67.0 +/- 6.2 years). 534 incident cancers with 152 cancer deaths and 409 all-cause deaths were recorded after a median follow-up of 6 years. Intake of simple sugars in solid form was unrelated to outcomes. Higher cancer incidence was found per 5 g/day increase in intake of liquid sugars, with multivariable-adjusted HR of 1.08 (95% CI, 1.03-1.13) for total liquid sugar, 1.19 (95% CI, 1.07-1.31) for liquid glucose, 1.14 (95% CI, 1.05-1.23) for liquid fructose, and 1.39 (95% CI, 1.10-1.74) for fructose from fruit juice. Cancer and all-cause mortality increased to a similar extent with intake of all sugars in liquid form. In categorical models, cancer risk was dose-related for all liquid sugars. Conclusions: Simple sugar intake in drinks and fruit juice was associated with an increased risk of overall cancer incidence and mortality and all-cause mortality. This suggests that sugary beverages are a modifiable risk factor for cancer and all-cause mortality. (c) 2021 The Authors. Published by Elsevier Ltd. This is an open access research article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).