Aims
Obesity suppresses brain‐derived neurotrophic factor (BDNF) expression and increases the expression of pro‐inflammatory cytokines. Herein, we assessed whether exercise training (ET), melatonin administration (MT), or their combination can affect the expressions of BDNF and cytokines in the cerebellum of high‐fat diet (HFD)‐fed rats.
Methods
Wistar rats (4 weeks old) were divided into five groups: normal diet (ND)‐fed control (ND‐SED), HFD‐fed control (HFD‐SED), HFD‐fed ET (HFD‐ET), HFD‐fed MT (HFD‐MT), and HFD‐fed MT plus ET (HFD‐ETMT) group. The rats were fed ND or HFD for 17 weeks. Rats were subjected to ET (running on a treadmill) and/or MT (melatonin 5 mg/kg body weight, i.p.) for 9 weeks, 8 weeks after beginning the diet intervention. Changes in BDNF and cytokine expression levels were determined using immunoblotting and cytokine arrays, respectively, 36 hours following the last bout of ET.
Results
Neither HFD‐ET nor HFD‐MT rats exhibited enhanced BDNF expression in the cerebellum, but HFD‐ETMT rats had higher level of BDNF expression compared with the others. The expression of TrkB, a BDNF receptor, was higher in HFD‐ETMT rats than in HFD‐ET and HFD‐MT rats. HFD enhanced the expression of interleukin (IL)‐1, IL‐2, and interferon‐γ but reduced the expression of IL‐4, IL‐6, and IL13. ET and ET plus MT counteracted these HFD‐induced changes in cytokine expressions.
Conclusion
Exercise in combination with melatonin confers the potential benefits of increasing BDNF and improving HFD‐induced dysregulations of cytokines in the cerebellum.
Summary
Recent evidence suggests that short‐term obstructive sleep apnea (OSA) treatment could affect OSA pathogenesis such as ventilatory control. The aim of our present study was to identify the impact of long‐term treatment on the change in pathogenesis and natural progression of OSA. In a longitudinal analysis of a non‐obese cohort study, patients with OSA treated with either continuous positive airway pressure (CPAP) or an oral appliance (OA), interrupted their treatment for 1 week and underwent a polysomnography (PSG) off treatment that was compared with their initial PSG taken 5 years before treatment initiation. In all, 154 consecutive patients with OSA who were treated by CPAP using an auto‐titrating continuous positive airway pressure device (CPAP‐APAP) (n = 112), or by OA (n = 27) or were untreated (n = 15), PSG was performed twice with a median (range) follow‐up of 93 (60–176) months. Multivariate logistic regression showed that reduction of body mass index (BMI) and good treatment adherence to be significant predictors of favourable OSA progression, as represented by an improved or unchanged apnea–hypopnea index (AHI) (odds ratios were 5.14 and 2.89, respectively). Amongst the patients with an unchanged BMI and good CPAP‐APAP adherence (n = 55), the improvement in AHI was significantly associated with the decrease in supine non‐rapid eye movement‐AHI and mixed apnoea index/apnoea index, which are generally recognised to be determinants of ventilator instability. These findings suggest that not only weight but also treatment adherence are determinants in the natural progression of OSA severity.
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