Examinando por Autor "Casals, Cristina"

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Impact of the FTO Gene Variation on Appetite and Fat Oxidation in Young Adults
(MDPI, 2023-04-23) Ponce-Gonzalez, Jesús G; Martínez-Ávila, Ángel; Velázquez-Díaz, Daniel; Perez-Bey, Alejandro; Gómez-Gallego, Félix; Marín-Galindo, Alberto; Corral-Pérez, Juan; Casals, Cristina
The FTO rs9939609 gene, which presents three polymorphisms (AA, AT, and TT), has been associated with the development of obesity through an increased fat accumulation; however, the associations of the gene with other physiological mechanisms, such as appetite or fat oxidation, are still unclear. Therefore, this study aims to evaluate the influence of the FTO rs9939609 gene on different obesity-related factors in young adults. The FTO rs9939609 polymorphism was genotyped in 73 participants (28 women, 22.27 ± 3.70 years). Obesity-related factors included dietary assessment, physical activity expenditure, body composition, appetite sensation, resting metabolic rate, maximal fat oxidation during exercise (MFO), and cardiorespiratory fitness. Our results showed that TT allele participants expressed higher values of hunger (p = 0.049) and appetite (p = 0.043) after exercising compared to the AT allele group. Moreover, the TT allele group showed significantly higher values of MFO (p = 0.031) compared to the AT group, regardless of sex and body mass index. Thus, our results suggest that the FTO rs9939609 gene has an influence on appetite, hunger, and fat oxidation during exercise, with TT allele participants showing significantly higher values compared to the AT allele group. These findings may have practical applications for weight loss and exercise programs.
Lung Surfactant Lipids Provide Immune Protection Against Haemophilus influenzae Respiratory Infection
(Frontiers Media, 2019-03-18) García-Fojeda, Balén; González-Carnicero, Zoe; de Lorenzo, Alba; Minutti, Carlos M.; de Tapia, Lidia; Euba, Begoña; Iglesias-Ceacero, Alba; Castillo-Lluva, Sonia; Garmendia, Junkal; Casals, Cristina
Non-typeable Haemophilus influenzae (NTHi) causes persistent respiratory infections in patients with chronic obstructive pulmonary disease (COPD), probably linked to its capacity to invade and reside within pneumocytes. In the alveolar fluid, NTHi is in contact with pulmonary surfactant, a lipoprotein complex that protects the lung against alveolar collapse and constitutes the front line of defense against inhaled pathogens and toxins. Decreased levels of surfactant phospholipids have been reported in smokers and patients with COPD. The objective of this study was to investigate the effect of surfactant phospholipids on the host-pathogen interaction between NTHi and pneumocytes. For this purpose, we used two types of surfactant lipid vesicles present in the alveolar fluid: (i) multilamellar vesicles (MLVs, > 1μm diameter), which constitute the tensioactive material of surfactant, and (ii) small unilamellar vesicles (SUVs, 0.1μm diameter), which are generated after inspiration/expiration cycles, and are endocytosed by pneumocytes for their degradation and/or recycling. Results indicated that extracellular pulmonary surfactant binds to NTHi, preventing NTHi self-aggregation and inhibiting adhesion of NTHi to pneumocytes and, consequently, inhibiting NTHi invasion. In contrast, endocytosed surfactant lipids, mainly via the scavenger receptor SR-BI, did not affect NTHi adhesion but inhibited NTHi invasion by blocking bacterial uptake in pneumocytes. This blockade was made possible by inhibiting Akt phosphorylation and Rac1 GTPase activation, which are signaling pathways involved in NTHi internalization. Administration of the hydrophobic fraction of lung surfactant in vivo accelerated bacterial clearance in a mouse model of NTHi pulmonary infection, supporting the notion that the lipid component of lung surfactant protects against NTHi infection. These results suggest that alterations in surfactant lipid levels in COPD patients may increase susceptibility to infection by this pathogen.