Food addiction (FA) has gained more scientific attention but needs deeper understanding. Data indicates that the central melanocortin (MC) system through the MC4 receptor (MC4R) and its polymorphisms Show more
Food addiction (FA) has gained more scientific attention but needs deeper understanding. Data indicates that the central melanocortin (MC) system through the MC4 receptor (MC4R) and its polymorphisms play a crucial role in the regulation of eating behaviour and in the motivation for the rewarding properties of food potentially leading to obesity. This may also contribute to the emergence of altered reward-related behaviors such as FA. The study aims to evaluate the genetic contribution of rs17782313, rs12970134, rs10871777, rs6567160, rs17700144 MC4R polymorphisms to the development of FA and to assess the association between these MC4R variations and clinical features. Eating (EDE-Q, BES, NEQ, GQ) and general psychopathology (BDI-II, STAI-S, DERS) were evaluated in patients with obesity with and without FA. Y-FAS 2.0 was used to assess FA. A blood sample was collected from all patients for the genotyping of MC4R polymorphisms. All the polymorphisms were equally distributed between groups except for rs17782313. A direct association between rs17782313 with FA was evident. Patients with FA and with C allele showed higher risk of FA compared to group without FA. There was a significant effect of rs17782313 on psychopathological variables in patients with FA. Allele C carriers exhibited higher anxiety and depression than T carriers. The rs17782313 of the MC4R showed an association with FA. A significant direct influence of C allele on anxiety and depression emerged in the group with FA but not in patients without FA. Show less
Intermittent hypoxia is a key factor in inducing chronic systemic inflammation in obstructive sleep apnea (OSA), providing the molecular substrate for the development of a range of associated diseases Show more
Intermittent hypoxia is a key factor in inducing chronic systemic inflammation in obstructive sleep apnea (OSA), providing the molecular substrate for the development of a range of associated diseases. Variations in blood oxygen levels are known to cause epigenetic changes, including modulation of non-coding RNAs. We sought to investigate whether selected hypoxia-associated non-coding RNAs, i.e. miR-210-3p, miR-139-3p, MALAT1, and BACE1-AS, could be modulated by ventilatory therapy with continuous positive airway pressure (CPAP) in patients with moderate to severe OSA. Their relationships with respiratory indices was also evaluated. Peripheral blood was collected from 68 patients with OSA before (pre-CPAP group) and after a 6-month treatment with CPAP (post-CPAP group). Circulating microRNAs and long non-coding RNAs levels were measured by real-time qPCR. Respiratory indices during sleep were evaluated by polysomnography. Following CPAP, levels of miR-210-3p, MALAT1, and BACE1-AS decreased while those of miR-139-3p increased (P<0.05 for all). Correlations between non-coding RNAs and ventilatory indices before CPAP, particularly time below 90 % of oxygen saturation during sleep, were statistically significant (P<0.05 for miR-210-3p, MALAT1, and miR-139-3p). Interestingly, all correlations were abolished by ventilation therapy. We conclude that CPAP therapy can modulate hypoxia-associated non-coding RNAs by restoring adequate blood oxygen levels, with potential effects on target gene expression. We speculate that non-coding RNAs may play a role in the development of OSA-related disorders such as cancer and cognitive diseases. Show less