Examination of food consumption in United States adults and the prevalence of inflammatory bowel disease using National Health Interview Survey 2015.

Various diets and food components have been implicated as one of the environmental factors associated with inflammatory bowel disease (IBD). Patients are often recommended nutritional guidelines to manage disease symptoms. However, the current food consumption pattern of US adults with IBD that are nationally representative is unclear. A secondary analysis of National Health Interview Survey 2015 was performed to characterize the estimated US adults with IBD and their food intake and consumption frequency using bivariate and multivariate logistic regression. Fries were consumed by a greater number of people with IBD. IBD population drank less 100% fruit juice and ate more cheese and cookies than non-IBD population. Intake of fries (OR 1.60, 95% CI 1.14-2.25) and sports and energy drinks (OR 1.46, 95% CI 1.07-1.97) and more frequent drinking of regular soda were significantly associated with the likelihood of having been told one have IBD, while popcorn (OR 0.73, 95% CI 0.548-0.971) and milk (OR 0.70, 95% CI 0.497-0.998) were associated with smaller odds, adjusting for covariates. Foods typically labeled as junk food were positively associated with IBD. Nonetheless, of the assessed 26 foods, we found eating patterns between IBD and non-IBD population to be mostly analogous. It is unclear whether the results reflect potential change in food intake in IBD population long before the survey interview. Understanding the role of food intake in IBD risk/prevalence would benefit from identifying other environmental factors (i.e. food desert), food processing (i.e. frying), and potential bioactive food components that can induce intestinal inflammation that can increase the individual's susceptibility to IBD.

Overexpression of CD98 in intestinal epithelium dysregulates miRNAs and their targeted proteins along the ileal villus-crypt axis.

CD98 has been implicated in the experimental model of inflammatory bowel disease. We have previously shown that IEC-specific overexpression of CD98 mediates intestinal inflammation and intestinal epithelial barrier dysfunction. Mice overexpressing CD98 exhibited severe colitis and a greater susceptibility to CAC. Here we demonstrated CD98 overexpression to dysregulate homeostatic gradient profile of miRNA and protein expression along the ileal villus-crypt axis. Using miRNA-target gene prediction module, we observed differentially expressed miRNAs to target proteins of villus and crypt profoundly affected by CD98 overexpression. We have utilized online bioinformatics as methods to further scrutinize the biological meanings of miRNA-target data. We identified significant interactions among the differentially regulated proteins targeted by altered miRNAs in Tg mice. The biological processes affected by the predicted targets of miRNAs deviate from the homeostatic functions of the miRNA-gene-protein axis of the wildtype mice. Our results emphasize a dynamic perturbation of miRNA and protein expression in villus-crypt axis contributing to potential biological consequences of altering CD98 expression. Our findings also suggest the need for a consideration of arrays of interacting biological entities (i.e. miRNAs-mRNAs, protein-protein interaction) or a combination comparison for a better understanding of the disease pathology which is necessary for an effective therapeutic target development.

Tauroursodeoxycholic Acid Protects Retinal Function and Structure in rd1 Mice.

We explored the potential protective effects of tauroursodeoxycholic acid (TUDCA) on cone photoreceptor survival in a model of rapid retinal degeneration, the ß-Pde6 (rd1) (rd1) mouse model. We injected two strains of rd1 mice (B6.C3-Pde6b (rd1) Hps4(le)/J and C57BL/6J-Pde6b (rd1-2)/J mice) daily from postnatal day (P) 6 to P21 with TUDCA or vehicle. At P21, retinal function was evaluated with light-adapted electroretinography (ERG) and retinal structure was observed with plastic or frozen sections. TUDCA treatment partially preserved function and structure in B6.C3-Pde6b (rd1) Hps4(le)/J mice but only partially preserved structure in C57BL/6J-Pde6b (rd1-2)/J mice. Our results suggest a possible intervention for patients undergoing rapid retinal degeneration.

Exercise and Cyclic Light Preconditioning Protect Against Light-Induced Retinal Degeneration and Evoke Similar Gene Expression Patterns.

To compare patterns of gene expression following preconditioning cyclic light rearing versus preconditioning aerobic exercise. BALB/C mice were preconditioned either by rearing in 800 lx 12:12 h cyclic light for 8 days or by running on treadmills for 9 days, exposed to toxic levels of light to cause light-induced retinal degeneration (LIRD), then sacrificed and retinal tissue harvested. Subsets of mice were maintained for an additional 2 weeks and for assessment of retinal function by electroretinogram (ERG). Both preconditioning protocols partially but significantly preserved retinal function and morphology and induced similar leukemia inhibitory factor (LIF) gene expression pattern. The data demonstrate that exercise preconditioning and cyclic light preconditioning protect photoreceptors against LIRD and evoke a similar pattern of retinal LIF gene expression. It may be that similar stress response pathways mediate the protection provided by the two preconditioning modalities.

Aerobic exercise protects retinal function and structure from light-induced retinal degeneration.

Aerobic exercise is a common intervention for rehabilitation of motor, and more recently, cognitive function (Intlekofer and Cotman, 2013; Wood et al., 2012). While the underlying mechanisms are complex, BDNF may mediate much of the beneficial effects of exercise to these neurons (Ploughman et al., 2007; Griffin et al., 2011; Real et al., 2013). We studied the effects of aerobic exercise on retinal neurons undergoing degeneration. We exercised wild-type BALB/c mice on a treadmill (10 m/min for 1 h) for 5 d/week or placed control mice on static treadmills. After 2 weeks of exercise, mice were exposed to either toxic bright light (10,000 lux) for 4 h to induce photoreceptor degeneration or maintenance dim light (25 lux). Bright light caused 75% loss of both retinal function and photoreceptor numbers. However, exercised mice exposed to bright light had 2 times greater retinal function and photoreceptor nuclei than inactive mice exposed to bright light. In addition, exercise increased retinal BDNF protein levels by 20% compared with inactive mice. Systemic injections of a BDNF tropomyosin-receptor-kinase (TrkB) receptor antagonist reduced retinal function and photoreceptor nuclei counts in exercised mice to inactive levels, effectively blocking the protective effects seen with aerobic exercise. The data suggest that aerobic exercise is neuroprotective for retinal degeneration and that this effect is mediated by BDNF signaling.

Dopamine deficiency contributes to early visual dysfunction in a rodent model of type 1 diabetes.

Dopamine (DA) functions as an essential neuromodulator in the brain and retina such that disruptions in the dopaminergic system are associated with common neurologic disorders such as Parkinson's disease. Although a reduction in DA content has been observed in diabetes, its effects in the development of diabetes-induced neuropathy remains unknown. Because the retina is rich in DA and has a well known diabetes-induced pathology (diabetic retinopathy or DR), this study was designed to examine the role of retinal DA deficiency in early visual defects in DR. Using rodent models of type 1 diabetes mellitus, we investigated whether diabetes caused a reduction in retinal DA content in both rats and mice and determined whether restoring DA levels or activating specific DA receptor pathways could improve visual function (evaluated with optokinetic tracking response) of diabetic mice, potentially via improvement of retinal function (assessed with electroretinography). We found that diabetes significantly reduced DA levels by 4 weeks in rats and by 5 weeks in mice, coincident with the initial detection of visual deficits. Treatment with l-DOPA, a DA precursor, improved overall retinal and visual functions in diabetic mice and acute treatment with DA D1 or D4 receptor agonists improved spatial frequency threshold or contrast sensitivity, respectively. Together, our results indicate that retinal DA deficiency is an underlying mechanism for early, diabetes-induced visual dysfunction and suggest that therapies targeting the retinal dopaminergic system may be beneficial in early-stage DR.