Dietary intake, weight status, pulmonary function, and metabolic profile in children with cystic fibrosis with or without pancreatic sufficiency.

OBJECTIVE: Nutritional status and growth is well associated with disease outcomes and lung function in patients with cystic fibrosis (CF). Current dietary guidelines for the management of CF suggest a high-calorie, high-fat diet. Pancreatic insufficiency (PI) is present in most patients and contributes to malabsorption and malnutrition, but a considerable number of patients have pancreatic sufficiency (PS). The aim of this study was to compare weight status, clinical characteristics, and dietary intake of children with CF, with PS or PI. METHODS: Patients with a diagnosis of CF (sweat test ≥60 mmol/L) and/or two known mutations for CF, ages 1 to 19 y were included in the study. Weight status, pulmonary characteristics, and blood lipid concentrations were evaluated. Dietary intake was evaluated through four 24-h recalls and energy, macronutrient intake, and intake in terms of food groups were assessed. RESULTS: Included in the present analyses were 134 patients with CF (30 with PS and 104 with PI). The percentage of overweight/obesity (47%) was higher in children with PS than in those with PI (22%). Overall, children with PS had higher body mass index, blood lipid levels, and pulmonary function levels than those with PI (all P < 0.05). Total energy intake was lower in children with PS than in those with PI (P < 0.001), even after adjustment for age and sex (Padj < 0.001). CONCLUSIONS: Weight status, dietary intake, pulmonary function, and lipid profile differed significantly in children with CF by pancreatic status. Nevertheless, the percentage of overweight and obesity was higher in children with PS than in those with PI. To avoid obesity, dietary recommendations for a high-calorie, high-fat diet should be reconsidered in patients with CF regarding their pancreatic status.

Effects of Dietary and Lifestyle Interventions on Liver, Clinical and Metabolic Parameters in Children and Adolescents with Non-Alcoholic Fatty Liver Disease: A Systematic Review.

Non-alcoholic fatty liver disease (NAFLD) affects 5.5-10.3% of children worldwide, while in obese individuals, it increases to almost 34%. Pediatric NAFLD is consistently associated with metabolic syndrome and insulin resistance. As no pharmacological agents exist for the treatment of NAFLD, lifestyle modifications remain the only therapy. However, as not all overweight/obese children have NAFLD, high-quality data, focused exclusively on NAFLD population are needed. Therefore, the present systematic review assessed the efficacy of lifestyle (diet or exercise) based on randomized controlled clinical trials (RCTs) on liver, anthropometric, glucose, and lipid parameters in children, with imaging or biopsy-proven NAFLD. In general, the results were inconclusive and therefore no specific recommendations could be drawn. In most studies, differences were derived from within group comparisons, which are known to be highly misleading. However, both low-carbohydrate and low-fat diets could benefit liver outcomes, as long as weight loss is achieved, but not necessary glucose and lipid parameters. No RCTs were found on exercise alone, as compared to no intervention on pediatric NAFLD. Concerning diet plus exercise interventions, all studies led to improvements in liver outcomes accompanied with weight loss. Resolution of NAFLD was found in considerably high percentages, while improvements were also seen in glucose but were modest in lipid parameters.

Inflammation associated ethanolamine facilitates infection by Crohn's disease-linked adherent-invasive Escherichia coli.

BACKGROUND: The predominance of specific bacteria such as adherent-invasive Escherichia coli (AIEC) within the Crohn's disease (CD) intestine remains poorly understood with little evidence uncovered to support a selective pressure underlying their presence. Intestinal ethanolamine is however readily accessible during periods of intestinal inflammation, and enables pathogens to outcompete the host microbiota under such circumstances. METHODS: Quantitative RT-PCR (qRT-PCR) to determine expression of genes central to ethanolamine metabolism; transmission electron microscopy to detect presence of bacterial microcompartments (MCPs); in vitro infections of both murine and human macrophage cell lines examining intracellular replication of the AIEC-type strain LF82 and clinical E. coli isolates in the presence of ethanolamine; determination of E. coli ethanolamine utilization (eut) operon transcription in faecal samples from healthy patients, patients with active CD and the same patients in remission following treatment. RESULTS: Growth on the intestinal short chain fatty acid propionic acid (PA) stimulates significantly increased transcription of the eut operon (fold change relative to glucose: >16.9; p-value <.01). Additionally ethanolamine was accessible to intra-macrophage AIEC and stimulated significant increases in growth intracellularly when it was added extracellularly at concentrations comparable to those in the human intestine. Finally, qRT-PCR indicated that expression of the E. coli eut operon was increased in children with active CD compared to healthy controls (fold change increase: >4.72; P < .02). After clinical remission post-exclusive enteral nutrition treatment, the same CD patients exhibited significantly reduced eut expression (Pre vs Post fold change decrease: >15.64; P < .01). INTERPRETATION: Our data indicates a role for ethanolamine metabolism in selecting for AIEC that are consistently overrepresented in the CD intestine. The increased E. coli metabolism of ethanolamine seen in the intestine during active CD, and its decrease during remission, indicates ethanolamine use may be a key factor in shaping the intestinal microbiome in CD patients, particularly during times of inflammation. FUND: This work was funded by Biotechnology and Biological Sciences Research Council (BBSRC) grants BB/K008005/1 & BB/P003281/1 to DMW; by a Tenovus Scotland grant to MJO; by Glasgow Children's Hospital Charity, Nestle Health Sciences, Engineering and Physical Sciences Research Council (EPSRC) and Catherine McEwan Foundation grants awarded to KG; and by a Natural Environment Research Council (NERC) fellowship (NE/L011956/1) to UZI. The IBD team at the Royal Hospital for Children, Glasgow are supported by the Catherine McEwan Foundation and Yorkhill IBD fund. RKR and RH are supported by NHS Research Scotland Senior fellowship awards.