Anorexia nervosa (AN) is a psychiatric disease with devastating physical consequences, with a pathophysiological mechanism still to be elucidated. Metagenomic studies on anorexia nervosa have revealed profound gut microbiome perturbations as a possible environmental factor involved in the disease. In this study we performed a comprehensive analysis integrating data on gut microbiota with clinical, anthropometric and psychological traits to gain new insight in the pathophysiology of AN. Fifteen AN women were compared with fifteen age-, sex- and ethnicity-matched healthy controls. AN diet was characterized by a significant lower energy intake, but macronutrient analysis highlighted a restriction only in fats and carbohydrates consumption. Next generation sequencing showed that AN intestinal microbiota was significantly affected at every taxonomic level, showing a significant increase of Enterobacteriaceae, and of the archeon Methanobrevibacter smithii compared with healthy controls. On the contrary, the genera Roseburia, Ruminococcus and Clostridium, were depleted, in line with the observed reduction in AN of total short chain fatty acids, butyrate, and propionate. Butyrate concentrations inversely correlated with anxiety levels, whereas propionate directly correlated with insulin levels and with the relative abundance of Roseburia inulinivorans, a known propionate producer. BMI represented the best predictive value for gut dysbiosis and metabolic alterations, showing a negative correlation with Bacteroides uniformis (microbiota), with alanine aminotransferase (liver function), and with psychopathological scores (obsession-compulsion, anxiety, and depression), and a positive correlation with white blood cells count. In conclusion, our findings corroborate the hypothesis that the gut dysbiosis could take part in the AN neurobiology, in particular in sustaining the persistence of alterations that eventually result in relapses after renourishment and psychological therapy, but causality still needs to be proven.

Background: Many laboratories offer glycemic index (GI) services. Objective: We assessed the performance of the method used to measure GI. Design: The GI of cheese-puffs and fruit-leather (centrally provided) was measured in 28 laboratories (n = 311 subjects) by using the FAO/WHO method. The laboratories reported the results of their calculations and sent the raw data for recalculation centrally. Results: Values for the incremental area under the curve (AUC) reported by 54% of the laboratories differed from central calculations. Because of this and other differences in data analysis, 19% of reported food GI values differed by >5 units from those calculated centrally. GI values in individual subjects were unrelated to age, sex, ethnicity, body mass index, or AUC but were negatively related to within-individual variation (P = 0.033) expressed as the CV of the AUC for repeated reference food tests (refCV). The between-laboratory GI values (mean ± SD) for cheese-puffs and fruit-leather were 74.3 ± 10.5 and 33.2 ± 7.2, respectively. The mean laboratory GI was related to refCV (P = 0.003) and the type of restrictions on alcohol consumption before the test (P = 0.006, r² = 0.509 for model). The within-laboratory SD of GI was related to refCV (P < 0.001), the glucose analysis method (P = 0.010), whether glucose measures were duplicated (P = 0.008), and restrictions on dinner the night before (P = 0.013, r² = 0.810 for model). Conclusions: The between-laboratory SD of the GI values is ≈9. Standardized data analysis and low within-subject variation (refCV < 30%) are required for accuracy. The results suggest that common misconceptions exist about which factors do and do not need to be controlled to improve precision. Controlled studies and cost-benefit analyses are needed to optimize GI methodology. The trial was registered at clinicaltrials.gov as NCT00260858.

Objective: To investigate the effect of a breakfast cereal containing inulin on blood lipids and colonic ecosystem in normolipidemic young men. Setting: Department of Food Science and Microbiology,University of Milan, Italy. Subjects: Twelve healthy male volunteers, age 23.3±0.5 y, body mass index (BMI) 25.7±1.2 kg/m² (mean±s.e.m.). Interventions: Subjects consumed daily, for three periods of four weeks, 50 g of a rice-based ready-to-eat cereal (placebo) and the same cereal containing 18% inulin (test) in substitution of their habitual breakfast, then returned to the habitual diet (wash-out). They followed no other dietary restrictions. Results: No changes in body weight, dietary habits, faecal and bile acid output, faecal short-chain fatty acid (SCFA) and faecal pH, were observed at the end of each period, whereas plasma total cholesterol and triacylglycerols significantly decreased at the end of test period by 7.9±5.4 (P<0.05) and 21.2±7.8% (P<0.005) respectively. Meal glucose tolerance test (MTT) resulted in the same incremental area under the curve for both cereals (IAUC test 124±35; placebo 118±33 mmol·min/l, ns). Inulin markedly enhanced breath H₂ excretion (IAUC test 280±40; placebo 78±26 ppm·h, P<0.005), as well as faecal concentration of L-lactate. Total facultative anaerobes significantly decreased after test, and bifidobacteria increased after correction for total anaerobes (P<0.05). Changes in blood lipids were negatively correlated with bifidobacteria counts and positively with secondary bile acid excretion (P<0.05). Conclusions: Inulin seems to have a lipid lowering potential in normolipidemic men possibly mediated by mechanisms related to colonic fermentation. Sponsorship: National Research Council of Italy, grant number 95.00773.PF41.

Exogenous fibre added to liquid meals delays gastric emptying. Its effect on solid meals is uncertain, and nothing is known of the effect on gastric emptying of fibre naturally present in food. This study therefore looked at gastric emptying of two different solid meals in eight healthy subjects and their blood glucose responses. The meals were exactly equivalent except for the total dietary fibre content (high fibre 20 g, low fibre 4 g of dietary fibre per 1000 kcal) and supplied 870 kcal (700 kcal women), 47% of which was from carbohydrates, 36% from fats, and 17% from proteins. Ultrasonography was used to measure antral diameters before the meal (basal), immediately after it (time 0), and at 30, 60, 120, 180, 240, and 300 minutes. In addition, subjects filled in a questionnaire on their feelings of hunger, epigastric fullness, and satiety before the meal and at hourly intervals after it. Basal and maximal postprandial antral sections were similar for the two meals (basal section: 283.9 (29.5) v 340.9 (44.7) mm2 for the low and the high fibre meal, NS; maximal postprandial section: 1726 (101.9) v 1593 (120.4) mm2, NS). Total gastric emptying time was significantly reduced by fibre removal (186.0 (15.6) v 231.7 (17.3) minutes after the low and the high fibre meal, p < 0.05). Blood glucose was higher after the low fibre meal, and the area under the glycaemic curve significantly greater (226 (23.1) v 160 (20.0) mmol/min/dl-1, p < 0.05). No difference was found in satiety or fullness feelings, but hunger returned more rapidly after the low fibre meal. In conclusion, fibre naturally present in food delays gastric emptying of a solid meal, reduces the glycaemic response, and delays the return of hunger.