Publications by authors named "M J Beyak"

Background: Ulcerative colitis and Crohn's disease are subtypes of inflammatory bowel disease: a chronic condition of unclear etiology characterized by inflammation of the small and large intestine. Inflammatory bowel disease is managed with diet, medications, and surgeries, with the most common surgery, recommended to ulcerative colitis patients being j-pouch surgery.

Purpose: To assess the current literature concerning psychosocial factors associated with j-pouch surgery for patients with inflammatory bowel disease.

View Article and Find Full Text PDF

Vagal afferents convey signals of mechanical stimulation in the gut to the brain, which is essential for the regulation of food intake. However, ion channels sensing mechanical stimuli are not fully understood. This study aimed to examine the ionic currents activated by mechanical stimulation and a possible neuro-modulatory role of nitric oxide on vagal afferents.

View Article and Find Full Text PDF

Inflammatory bowel disease (IBD) is a painful chronic gastrointestinal disease associated with diminished quality of life. No research documents IBD body pain or the associations of pain patterns to outcomes. Objectives were to map patient body pain areas and examine the associations between pain patterns with depression, catastrophizing, pain severity, and quality of life.

View Article and Find Full Text PDF

The gut microbiota has been implicated in chronic pain disorders, including irritable bowel syndrome (IBS), yet specific pathophysiological mechanisms remain unclear. We showed that decreasing intake of fermentable carbohydrates improved abdominal pain in patients with IBS, and this was accompanied by changes in the gut microbiota and decreased urinary histamine concentrations. Here, we used germ-free mice colonized with fecal microbiota from patients with IBS to investigate the role of gut bacteria and the neuroactive mediator histamine in visceral hypersensitivity.

View Article and Find Full Text PDF

Background/objectives: Disrupted leptin signaling in vagal afferent neurons contributes to hyperphagia and obesity. Thus, we tested the hypothesis that intrinsic negative regulators of leptin signaling, suppressor of cytokine signaling 3 (SOCS3) and protein tyrosine phosphatase 1B (PTP1B) underlie dysfunctional leptin-mediated vagal afferent satiety signaling during obesity.

Methods: Experiments were performed on standard chow-fed control mice, high-fat fed (HFF), or low-fat fed (LFF) mice.

View Article and Find Full Text PDF