An Overview Of The Management And Rehabilitation Of Dysphagia.

Dysphagia is a medical condition that makes it difficult for a person to eat or swallow. It is estimated that 590 million people worldwide have dysphagia. The causes are varied and include neurological disorders like stroke and motor neuron disease, head and neck cancer, neuromuscular diseases, inflammatory diseases such as dermatomyositis, dementia, cervical spinal cord injury, and anterior vertebral ossification. The assessment and screening of dysphagia consists of a questionnaire-based interview, mealtime observation, and, if deemed necessary by a screening test or instrumental examination by specialists. Treatment is based on the diagnosis, patients' cognition and information gathered by screening and clinical evaluation. Patient's function can be improved only when treatment is comprehensive and includes compensatory feeding using an adjusted swallowing diet, compensatory posture adjustment, and nutritional improvement. We present a brief overview of the assessment and management strategies for dysphagia.

The Relationship between Low Skeletal Muscle Mass and Subsequent Oral Intake Ability among the Aged Population.

This study aimed to determine the relationship between skeletal muscle mass in an aged population with limited oral intake upon admission and functional oral intake at the subsequent 3-month follow-up. Methods: This was a retrospective cohort study using the Japanese Sarcopenia Dysphagia Database involving older adults (≥60 years) with limited oral intake (Food Intake Level Scale [FILS] level of ≤8). People without skeletal muscle mass index (SMI) data, unknown methods of SMI evaluation, and SMI evaluation by DXA were excluded. Data for 76 people (47 women, 29 men) were analyzed (mean [standard deviation] age: 80.8 [9.0] years; median SMI: women, 4.80 kg/m2; men, 6.50 kg/m2). There were no significant differences in age, FILS upon admission and methods of nutrition intake between the low (n = 46) and the high skeletal muscle mass groups (n = 30), although the proportion of sex between the two groups was different. The FILS level at the time of follow-up differed significantly between the groups (p < 0.01). The SMI upon admission (odds ratio: 2.99, 95% confidence interval: 1.09-8.16) were significantly associated with the FILS level at the time of follow-up after adjustment for sex, age, and history of stroke and/or dementia (p < 0.05, power = 0.756). Conclusion: A low skeletal muscle mass is a disadvantage for achieving a subsequent fully functional oral intake ability among the aged population with limited oral intake upon admission.

Bile acid binding resin prevents fat accumulation through intestinal microbiota in high-fat diet-induced obesity in mice.

BACKGROUND: Bile acid binding resin (BAR) absorbs intestinal bile acids, and improves obesity and metabolic disorders, but the precise mechanism remains to be clarified. Recent findings reveal that obesity is associated with skewed intestinal microbiota. Thus, we investigated the effect of BAR on intestinal microbiota and the role of microbiota in the prevention of obesity in high-fat diet-induced obesity in mice. PROCEDURES: Male Balb/c mice were fed a low-fat diet (LFD), high-fat diet (HFD), or HFD with BAR (HFD+BAR), and then metabolic parameters, caecal microbiota, and metabolites were investigated. The same interventions were conducted in germ-free and antibiotic-treated mice. MAIN FINDINGS: The frequency of Clostridium leptum subgroup was higher in both HFD-fed and HFD+BAR-fed mice than in LFD-fed mice. The frequency of Bacteroides-Prevotella group was lower in HFD-fed mice than in LFD-fed mice, but the frequency was higher in HFD+BAR-fed mice than in HFD-fed mice. Caecal propionate was lower in HFD-fed mice than in LFD-fed mice, and higher in HFD+BAR-fed mice than in HFD-fed mice. HFD+BAR-fed mice showed lower adiposity than HFD-fed mice, and the reduction was not observed in germ-free or antibiotic-treated mice. Colonized germ-free mice showed a reduction in adiposity by BAR administration. Energy expenditure was lower in HFD-fed mice and higher in HFD+BAR-fed mice, but the increments induced by administration of BAR were not observed in antibiotic-treated mice. CONCLUSIONS: Modulation of intestinal microbiota by BAR could be a novel therapeutic approach for obesity.

GLP-1 receptor agonist, liraglutide, ameliorates hepatosteatosis induced by anti-CD3 antibody in female mice.

AIMS: Hepatosteatosis is mainly induced by obesity and metabolic disorders, but various medications also induce hepatosteatosis. The administration of anti-CD3 antibody was shown to induce hepatosteatosis, but changes in lipid and glucose metabolism remain unclear. We investigated the mechanism of hepatosteatosis induced by anti-CD3 antibody and the effects of glucagon-like peptide-1 (GLP-1) receptor agonist that was recently shown to affect immune function in metabolic disorders. METHODS: Anti-CD3 antibody was administered to female BALB/c and C.B-17-scid mice with or without reconstitution by naïve CD4-positive splenocytes. Hepatic lipid content, serum lipid profile and glucose tolerance were evaluated. Splenic CD4-positive T lymphocytes were stimulated with the GLP-1R agonist, liraglutide, and cytokine production was measured. The effect of liraglutide on metabolic parameters in vivo was investigated in a T-cell activation-induced hepatosteatosis model. RESULTS: The administration of anti-CD3 antibody induced hepatosteatosis, hyperlipidemia, and glucose intolerance. C.B-17-scid mice reconstituted with CD4-positive T lymphocytes developed hepatosteatosis induced by anti-CD3 antibody. Liraglutide suppressed CD4-positive T lymphocyte cytokine expression in vitro and in vivo, and improved hepatosteatosis, glucose tolerance, and insulin sensitivity. CONCLUSIONS: Liraglutide suppressed the activation of CD4-positive T lymphocytes, and improved hepatosteatosis and metabolic disorders induced by T-cell activation in female mice.

Bile acid binding resin improves hepatic insulin sensitivity by reducing cholesterol but not triglyceride levels in the liver.

AIMS: Bile acid binding resin (BAR) improves glycaemic control in patients with type 2 diabetes. Although the mechanism is hypothesised to involve the clearance of excess hepatic triglyceride, this hypothesis has not been examined in appropriately designed studies. Therefore, we investigated whether reduced hepatic triglyceride deposition is involved in BAR-mediated improvements in glycaemic control in spontaneous fatty liver diabetic mice without dietary interventions. METHODS: Male 6-week-old fatty liver Shionogi (FLS) mice were fed a standard diet without or with 1.5% BAR (colestilan) for 6 weeks. Glucose tolerance, insulin sensitivity, hepatic lipid content, and gene expression were assessed. A liver X receptor (LXR) agonist was also administered to activate the LXR pathway. We also retrospectively analysed the medical records of 21 outpatients with type 2 diabetes who were treated with colestilan for ≥6 months. RESULTS: BAR enhanced glucose tolerance and insulin sensitivity in FLS mice without altering fat mass. BAR improved hepatic insulin sensitivity, increased IRS2 expression, and decreased SREBP expression. BAR reduced hepatic cholesterol levels but not hepatic triglyceride levels. BAR also reduced the expression of LXR target genes, and LXR activation abolished the BAR-mediated improvements in glycaemic control. Colestilan significantly lowered serum cholesterol levels and improved glycaemic control in patients with type 2 diabetes. CONCLUSIONS: BAR improved hepatic insulin resistance in FLS mice by reducing hepatic cholesterol without affecting hepatic triglyceride levels or body fat distribution. Our study revealed that BAR improves glycaemic control at least in part by downregulating the hepatic cholesterol-LXR-IRS2 pathway.