Abnormal food timing and predisposition to weight gain: Role of barrier dysfunction and microbiota.

Obesity has become a common rising health care problem, especially in "modern" societies. Obesity is considered a low-grade systemic inflammation, partly linked to leaky gut. Circadian rhythm disruption, a common habit in modern life, has been reported to cause gut barrier impairment. Abnormal time of eating, defined by eating close to or during rest time, is shown to cause circadian rhythm disruption. Here, using a non-obesogenic diet, we found that abnormal feeding time facilitated weight gain and induced metabolic dysregulation in mice. The effect of abnormal time of eating was associated with increased gut permeability, estimated by sucralose and/or lactulose ratio and disrupted intestinal barrier marker. Analysis of gut microbiota and their metabolites, as important regulators of barrier homeostasis, revealed that abnormal food timing reduced relative abundance of butyrate-producing bacteria, and the colonic butyrate level. Overall, our data supported that dysbiosis was characterized by increased intestinal permeability and decreased beneficial barrier butyrate-producing bacteria and/or metabolite to mechanistically link the time of eating to obesity. This data provides basis for noninvasive microbial-targeted interventions to improve intestinal barrier function as new opportunities for combating circadian rhythm disruption induced metabolic dysfunction.

Prevalence of allergic rhinitis and asthma in patients with chronic rhinosinusitis and gastroesophageal reflux disease.

BACKGROUND: An association between chronic rhinosinusitis (CRS) and gastroesophageal reflux disease (GERD) has been previously reported; however, the underlying factors linking CRS and GERD remain to be elucidated. OBJECTIVE: To assess the association of GERD and CRS using prospective and retrospective approaches. METHODS: The retrospective study comprised a large cohort of CRS cases, whereas the prospective arm evaluated a series of CRS cases and controls. RESULTS: In the retrospective arm of the study, of the 1066 patients with CRS, 112 (10.5%) had GERD. Among patients with CRS, GERD was associated with higher body mass index, older age, and female sex. The odds ratios (ORs) for asthma and allergic rhinitis in the CRS group with GERD compared with the CRS group without GERD were 2.89 (95% confidence interval [CI], 1.905-4.389) and 2.021 (95% CI, 1.035-3.947). Furthermore, GERD was associated with a greater duration of CRS. Ninety patients with CRS and 81 controls were enrolled in the prospective arm of the study. In the CRS group, GERD was associated with asthma (OR, 4.77; 95% CI, 1.27-18.01). Patients with CRS and GERD had a longer duration and a younger age at onset of CRS. In controls, no association was found between GERD and asthma (OR, 0.67; 95% CI, 0.09-5.19) or allergic rhinitis (OR, 0.35; 95% CI, 0.05-2.59). CONCLUSION: Patients with CRS and GERD are more likely to have atopic conditions and asthma when compared with patients with CRS but without GERD. One of the potential explanations of this link is that comorbid GERD and atopic disease are potential risk factors for development of CRS.