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Summary Background & aims The resting energy expenditure (REE) predictive formulas are often used in clinical practice to adapt the nutritional intake of patients or to compare to REE measured by indirect calorimetry. We aimed to evaluate which predictive equations was the best alternative to REE measurements according to the BMI. Methods 28 REE prediction equations were studied in a population of 1726 patients without acute or chronic high-grade inflammatory diseases followed in a Nutrition Unit for malnutrition, eating disorders or obesity. REE was measured by indirect calorimetry for 30 min after a fasting period of 12 h. Some formulas requiring fat mass and free-fat mass, body composition was measured by bioelectrical impedance analysis. The percentage of accurate prediction (±10%/REE measured) and Pearson r correlations were calculated. Results Original Harris & Benedict equation provided 73.0% of accurate predictions in normal BMI group but only 39.3% and 62.4% in patients with BMI < 16 kg m −2 and BMI ≥ 40 kg m −2 , respectively. In particularly, this equation overestimated the REE in 51.74% of patients with BMI < 16 kg m −2 . Huang equation involving body composition provided the highest percent of accurate prediction, 42.7% and 66.0% in patients with BMI < 16 and >40 kg m −2 , respectively. Conclusion Usual predictive equations of REE are not suitable for predicting REE in patients with extreme BMI, in particularly in patients with BMI <16 kg m −2 . Indirect Calorimetry may still be recommended for an accurate assessment of REE in this population until the development of an adapted predictive equation. [ABSTRACT FROM AUTHOR]

Plasma levels of ghrelin, an orexigenic peptide, are increased during conditions of chronic starvation, such as in patients with anorexia nervosa. However, it is not known whether such increase can be related to the number of preproghrelin mRNA-expressing cells in the stomach, and if chronic starvation may activate a tentative central ghrelin production. In this work, in situ hybridization technique was used to analyze the presence and number of preproghrelin mRNA-expressing cells in the stomach and the hypothalamus of mice with activity-based anorexia (ABA) induced by the combination of running wheel activity with progressive, during 10 days, feeding-time restriction (FTR) and compared with sedentary FTR, ABA pair-fed (PF) and ad libitum -fed control mice. All food-restricted mice lost more than 20% of body weight. Body weight loss was similar in ABA and PF mice, but it was more pronounced than in FTR mice. Food intake was also lower in ABA than in FTR mice. Preproghrelin mRNA-expressing cells in the stomach were increased proportionally to the body weight loss in all food-restricted groups with the highest number in ABA mice. No preproghrelin mRNA-producing cells were detectable in the hypothalamus of either control or food-restricted mice. Thus, the increased number of gastric preproghrelin mRNA-producing cells during chronic starvation proportionally to the body weight loss and reduced food intake may underlie increased plasma ghrelin. Hyperactivity-induced anorexia appears to further increase the number of preproghrelin mRNA-producing cells in the stomach. No evidence was found for ghrelin expression in the hypothalamus, not even in any of the present experimental models. [ABSTRACT FROM AUTHOR]

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Summary Background & aims Anorexia nervosa is a severe eating disorder often leading to malnutrition and cachexia, but its pathophysiology is still poorly defined. Chronic food restriction during anorexia nervosa may induce gut barrier dysfunction, which may contribute to disease development and its complications. Here we have characterized intestinal barrier function in mice with activity-based anorexia (ABA), an animal model of anorexia nervosa. Methods Male C57Bl/6 ABA or limited food access (LFA) mice were placed respectively in cages with or without activity wheel. After 5 days of acclimatization, both ABA and LFA mice had progressively limited access to food from 6 h/d at day 6 to 3 h/d at day 9 and until the end of experiment at day 17. A group of pair-fed mice (PF) was also compared to ABA. Results On day 17, food intake was lower in ABA than LFA mice (2.0 ± 0.18 g vs. 3.0 ± 0.14 g, p < 0.001) and weight loss was more pronounced in ABA and PF compared to LFA mice (23.6 ± 1.6% and 24.7 ± 0.7% vs. 16.5 ± 1.2%; p < 0.05). Colonic histology showed decreased thickness of the muscularis layer in ABA compared to LFA mice ( p < 0.05). Colonic permeability was increased in both ABA and PF compared to LFA mice ( p < 0.05) but jejunal paracellular permeability was not affected. Expression of claudin-1 in the colon was lower in the ABA than the LFA group ( p < 0.05), whereas occludin expression remained unaffected. Conclusion Increased colonic permeability and histological alterations found in ABA mice suggest that intestinal barrier dysfunction may also occur in anorexia nervosa. The role of these alterations in the pathophysiology of anorexia nervosa should be further evaluated. [ABSTRACT FROM AUTHOR]

Summary: Background & aims: Increased intestinal permeability occurs during chemotherapy-induced intestinal mucositis. Previous data suggest that glutamine and arginine may have additive or synergic effects to limit intestinal damage. The present study aimed to evaluate the effects of glutamine and arginine, each alone or in combination, on gut barrier function during methotrexate (MTX)-induced mucositis in rats. Methods: Eighty Sprague Dawley rats received during 7 days (d) standard chow supplemented with protein powder (PP), glutamine (G, 2%), arginine (A, 1.2%) or glutamine plus arginine (GA). All diets were isonitrogenous. Rats received subcutaneous injections of MTX (2.5 mg/kg) from d0 to d2. The intestinal permeability and tight junction proteins were assessed at d4 and d9 in the jejunum by FITC-dextran and by western blot and immunohistochemistry, respectively. Results: At d4, intestinal permeability was increased in MTX-PP, MTX-A and MTX-GA rats compared with controls but not in MTX-G rats. The expression of claudin-1, occludin and ZO-1 was decreased in MTX-PP group compared with controls but was restored in MTX-G and MTX-A rats. In MTX-GA rats, occludin expression remained decreased. These effects could be explained by an increase of erk phosphorylation and a decrease of IκBα expression in MTX-PP and MTX-GA rats. At d9, Intestinal permeability remained higher only in MTX-GA rats. This was associated with a persistent decrease of occludin expression. Conclusions: Glutamine prevents MTX-induced gut barrier disruption by regulating occludin and claudin-1 probably through erk and NF-κB pathways. In contrast, combined glutamine and arginine has no protective effect in this model. [Copyright &y& Elsevier]

Abstract: Anti-α-melanocyte-stimulating hormone (α-MSH) polyclonal antibodies have been used for α-MSH neutralization in functional studies, but the results are sometime inconsistent with the antibody expected blocking properties. The present study aimed to determine if rabbit (Rb) anti-α-MSH immunoglobulins (Ig) may inhibit or enhance α-MSH signaling on melanocortin receptor type 4 (MC4R) and α-MSH-induced anorexigenic effect if presented as immune complexes with α-MSH. Polyclonal Rb anti-α-MSH IgG were commercially available and their ability to bind α-MSH has been confirmed by the immunohistochemical detection of α-MSH neurons in the rat hypothalamus. In vitro assay of the cyclic-adenosine mono-phosphate (cAMP) secreted by cells transfected with MC4R was performed to analyze effect of Rb IgG on α-MSH-induced cAMP production. We found that adding Rb IgG to α-MSH resulted in stimulation of cAMP detected at lower peptide concentrations as compared to α-MSH alone. To determine effects of Rb IgG on food intake, rats were injected into the arcuate hypothalamic nucleus with either α-MSH, Rb IgG alone or Rb IgG preincubated with α-MSH. During 2days after injections, food intake was increased in both groups of rats receiving Rb IgG. However, during following 4days when food was restricted to 1h/day, only the Rb IgG group displayed higher food intake. Furthermore, after the refeeding, 24h food intake was lower in rats receiving Rb IgG - α-MSH immune complexes. This group of rats was also characterized by higher number of immunopositive neurons in the arcuate nucleus expressing α-MSH and agouti-related protein but not tyrosine hydroxylase. Taken together, these results show that Rb anti-α-MSH antisera, although efficient for immunohistochemical detection of α-MSH, does not always display α-MSH blocking properties but, in contrast, may enhance α-MSH binding to MC4R and increase α-MSH anorexigenic effects when presented as immune complexes with the peptide. [Copyright &y& Elsevier]

Summary: Background & aims: Chemotherapy induces an increase of intestinal permeability that is partially related to an alteration of tight junction proteins, occludin and zonula occludens-1 (ZO-1). Protective effects of glutamine on intestinal barrier function have been previously shown but the effects of other amino acids remained poorly documented. Thus, we aimed to evaluate the effects of nine amino acids on intestinal permeability during methotrexate (MTX) treatment in Caco-2 cells. Methods: Caco-2 cells were incubated in culture medium supplemented with glutamine, arginine, glutamate, leucine, taurine, citrulline, glycine, histidine or cysteine during 24 h and then treated with MTX (100 ng/ml). The dose of each amino acid was 16.6 fold the physiological plasma concentrations. Barrier function was assessed by transepithelial electrical resistance (TEER), FITC-dextran paracellular flux, occludin and ZO-1 expression and localization. Signaling pathways were also studied. Results: Only glutamine, glutamate, arginine and leucine reversed the decrease of TEER observed after MTX treatment (P < 0.05). Interestingly, the addition of 6-diazo-5-oxo-1-norleucine, an inhibitor of glutaminase, blunted the effect of glutamine on MTX-treated cells (P < 0.05). Glutamine and arginine combination restored TEER and FITC-dextran flux to a similar extent than glutamine alone. In addition, pretreatment of Caco-2 cells with glutamine and arginine, alone or combined, differently limited the decrease of ZO-1 and occludin expression (P < 0.05) and the alteration of their cellular distribution, through c-Jun N-terminal kinase (JNK), Extracellular signal-regulated kinase (ERK) and nuclear factor kappa B (NF-κB) pathways. Conclusions: Glutamine prevented MTX-induced barrier disruption in Caco-2 cells. Arginine also had protective effects but in a lesser extent. The effect of glutamine and arginine should be evaluated in vivo. [Copyright &y& Elsevier]

Summary: Background & aims: Increased intestinal permeability of Irritable bowel syndrome (IBS) patients has been recently associated with a decreased level of glutamine synthetase. Neonatal maternal deprivation (NMD) is considered as an IBS-like model. The aim of our study was to investigate whether early nutritional intervention with glutamine may attenuate the deleterious impact of early life stress on gut barrier function in NMD. Methods: 124 rat pups were separated from their dam 3 h daily during postnatal days 2–14, or left undisturbed (NS). Separated rats received by gavage either with alanyl-glutamine (GLN), an isonitrogenous amino acid mix (AA, control) or an equal amount of drinking water (H2O). Production of cytokines was measured by multiplex, expression of COX-2, PPARγ, tight junction proteins and TLR4 by western blot. Intestinal permeability was studied by Lactulose/Mannitol test. Results: Treatment of pups with GLN or AA abolished the decrease in body weight observed in NMD. Treatment with GLN decreased in the colon (i) TLR4 expression at D20, (ii) IL-2 and -10 productions at D60 (iii) protein expression of occludin at D20 compared to AA. GLN also decreased colon expression of COX2 and PPARγ at D60 compared to NS. Colon production of IFNγ is significantly reduced by GLN compared to H2O. No significant change in intestinal permeability was observed. Conclusions: These results showed that an early nutritional intervention with alanyl-glutamine specifically abolished the up-regulation of TLR4 expression in NMD. Glutamine may be evaluated as a potential treatment for IBS patients. [Copyright &y& Elsevier]

Summary: Background & aims: The role of endothelial cells in inflammatory bowel disease has been recently emphasized. Endothelial activation and expression of adhesion molecules are critical for leukocytes recruitment into the inflammatory wall. Compelling evidence demonstrated anti-inflammatory effects of long chain n-3 PUFA in inflammatory models. We previously showed that long chain n-3 PUFA (EPA and DHA) inhibited inflammatory response in epithelial and dendritic cells. As long chain n-3 PUFA treatment led to a decreased expression of adhesion molecules in endothelial cells from other organs, we have now investigated their effect on intestinal endothelial cells in vitro and in colitic rats. Methods: In vitro study: Primary culture of human intestinal microvascular endothelial cells (HIMEC) were pre-treated with DHA and then incubated with IL-1β. In vivo study: Colitis was induced in 2 groups at day0 by intrarectal injection of 2-4-6-trinitrobenzen sulfonic acid (TNBS). Rats received by gavage either fish oil, rich in EPA and DHA (TNBS+n-3) or an isocaloric isolipidic oil formula for 14 days. Results: DHA led to a decreased VCAM-1, TLR4, cyclooxygenase-2 and VEGFR2 expression and a decreased production of IL-6, IL-8 and GM-CSF and a reduced production of PGE 2 and LTB 4 (p < 0.001) in IL-1β-induced HIMEC. Similarly, dietary intervention with fish oil rich in EPA and DHA significantly decreased colon production of PGE 2 and LTB 4, endothelial VCAM-1 and VEGFR2 in rats with colitis. Conclusions: Data obtained from in vitro and in vivo studies reveal a potential anti-angiogenic role of long chain n-3 PUFA in intestinal endothelial cells. This protective effect of long chain n-3 PUFA may partly explain the observed benefit of dietary intake of long chain n-3 PUFA in IBD development. [Copyright &y& Elsevier]

Summary: Background & aims: Although eating disorders prevalence is increasing, they are often under diagnosed in cases of unspecific signs of malnutrition. Screening scales may allow earlier diagnosis and nutritional intervention. This study aimed to evaluate the validity of the French version (SCOFF-F) of the SCOFF questionnaire for the detection of eating disorders among a female patient population referred to a clinical nutrition unit. Methods: After answering the 5 dichotomous questions of the paper version of SCOFF-F, patients were evaluated by one eating disorders specialist blinded to questionnaire results, using the MINI and Diagnosis and Statistical Manual for Mental diseases (DSM-IV) criteria as a gold standard. Results: Patients with anorexia nervosa (n = 67) and with bulimia nervosa (n = 45) were assessed. Age-matched healthy female students (n = 114) served as control group. At a cut-off of two positive responses, the sensibility, specificity and the area under the curve of SCOFF-F were 94.6%, 94.7% and 97.9% respectively. Cohen’s kappa coefficient between SCOFF-F and MINI results was 89%. Conclusions: The results of this study confirm the reliability of SCOFF-F as a screening and diagnostic-facilitating test for eating disorders in a French-speaking female patient population. SCOFF-F should help professionals in clinical nutrition to achieve earlier diagnosis and care of eating disorder patients. [Copyright &y& Elsevier]