Crohn's disease (CD), one of the 2 major forms of inflammatory bowel disease (IBD), is a chronic inflammatory disorder of unknown etiology that primarily affects the gastrointestinal tract.¹ x 1 Hibi, T. and Ogata, H. Novel pathophysiological concepts of inflammatory bowel disease. J Gastroenterol. 2006; 41: 10–16 Google Scholar See all References ^{, 2} x 2 Podolsky, D.K. Inflammatory bowel disease. N Engl J Med. 2002; 347: 417–429 Google Scholar See all References Although CD can affect the entire gastrointestinal tract, the small intestine and colon are most commonly involved. Although after years of intensive research the etiology of CD remains unknown, significant progress in recent years has provided new insights. It has been considered that CD is a multifactorial disease composed of genetic backgrounds, environmental factors, and immunologic response. Recent advances in molecular biology and human genomic analysis have demonstrated several IBD susceptibility genes. Several IBD susceptibility genes have recently been identified in Western populations and, except for TNFSF15, appear to contribute to IBD risk in Asian patients.³ x 3 Hugot, J.P., Chamaillard, M., Zouali, H. et al. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. Nature. 2001; 411: 599–603 Google Scholar See all References ^{, 4} x 4 Ogura, Y., Bonen, D.K., Inohara, N. et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease. Nature. 2001; 411: 603–606 Google Scholar See all References ^{, 5} x 5 Peltekova, V.D., Wintle, R.F., Rubin, L.A. et al. Functional variants of OCTN cation transporter genes are associated with Crohn's disease. Nat Genet. 2004; 36: 471–475 Google Scholar See all References ^{, 6} x 6 Stoll, M., Corneliussen, B., Costello, C.M. et al. Genetic variation in DLG5 is associated with inflammatory bowel disease. Nat Genet. 2004; 36: 476–480 Google Scholar See all References ^{, 7} x 7 Yamazaki, K., McGovern, D., Ragoussis, J. et al. Single nucleotide polymorphisms in TNFSF15 confer susceptibility to Crohn's disease. Hum Mol Genet. 2005; 14: 3499–3506 Google Scholar See all References Potentially important environmental factors include smoking, diet, and intestinal flora.⁷ x 7 Yamazaki, K., McGovern, D., Ragoussis, J. et al. Single nucleotide polymorphisms in TNFSF15 confer susceptibility to Crohn's disease. Hum Mol Genet. 2005; 14: 3499–3506 Google Scholar See all References ^{, 8} x 8 Inoue, N., Tamura, K., Kinouchi, Y. et al. Lack of common NOD2 variants in Japanese patients with Crohn's disease. Gastroenterology. 2002; 123: 86–91 Abstract | Full Text | Full Text PDF | Scopus (383) | Google Scholar See all References ^{, 9} x 9 Lee, G.H., Kim, C.G., Kim, J.S. et al. Frequency analysis of NOD2 gene mutations in Korean patients with Crohn's disease. Korean J Gastroenterol. 2005; 45: 162–168 Google Scholar See all References Although CD was rare in Asian countries including Japan, the number of patients with CD in this region has increased during the past decade. One of the reasons for the change to a more Western pattern of intestinal disorders is thought to be due to a more Westernized diet. CD may develop as a dysregulated mucosal immune response to antigens derived from diet or intestinal flora.

Physiological conditions in humans affect plasma amino acid profiles that might have potential for medical use. Because the branched-chain amino acids (BCAAs) leucine, isoleucine and valine are used as medicines and supplements, we investigated the acute effects of individual BCAAs (10–90 mg/kg body weight) or mixed BCAAs ingested as a bolus on plasma amino acid profiles in young healthy men. Plasma leucine levels rapidly increased and peaked around 30 min after leucine ingestion. Concentrations of plasma isoleucine, valine and phenylalanine subsequently decreased after ingestion, and those of methionine and tyrosine tended to decrease. The effects of ingested leucine on other plasma amino acids were biphasic, being higher at lower doses (10–20 mg/kg body weight). Isoleucine or valine intake also caused corresponding plasma amino acid concentrations to rapidly elevate, and peaks at 30–40 min after ingestion were much higher than that of plasma leucine after leucine ingestion. However, the increase in plasma isoleucine and valine concentrations essentially did not affect those of other plasma amino acids. The rate of decline among peak plasma BCAA concentrations was the highest for leucine, followed by isoleucine and valine. Oral mixed BCAAs promoted the decline in plasma isoleucine and valine concentrations. These results suggest that plasma leucine is a regulator of the plasma concentrations of BCAAs, methionine and aromatic amino acids.

The consumption of monosodium glutamate (MSG) is advocated to elicit physiological and metabolic effects, yet these effects have been poorly investigated directly in humans and in particular in the postprandial phase. Thirteen healthy adults were supplemented for 6 days with a nutritional dose of MSG (2 g) or sodium chloride (NaCl) as control, following a crossover design. On the 7th day, they underwent a complete postprandial examination for the 6 h following the ingestion of the same liquid standard meal (700 kcal, 20% of energy as [¹⁵N]protein, 50% as carbohydrate, and 30% as fat) supplemented with MSG or NaCl. Real-ultrasound measures of antral area indicated a significant increased distension for the 2 h following the meal supplemented with MSG vs. NaCl. This early postprandial phase was also associated with significantly increased levels of circulating leucine, isoleucine, valine, lysine, cysteine, alanine, tyrosine, and tryptophan after MSG compared with NaCl. No changes to the postprandial glucose, insulin, glucagon-like peptide (GLP)-1, and ghrelin were noted between MSG- and NaCl-supplemented meals. Subjective assessments of hunger and fullness were neither affected by MSG supplementation. Finally, the postprandial fate of dietary N was identical between dietary conditions. Our findings indicate that nutritional dose of MSG promoted greater postprandial elevations of several indispensable amino acids in plasma and induced gastric distension. Further work to elucidate the possible sparing effect of MSG on indispensable amino acid first-pass uptake in humans is warranted. This trial was registered at clinicaltrials.gov as NCT00862017.

This study assessed the effect of continuous ingestion of monosodium l-glutamate (MSG) on cognitive function and dietary score in dementia patients. This was a single-blind, placebo-controlled trial involving 159 subjects with dementia residing in a hospital or nursing home. We assigned the subjects to a group that ingested MSG thrice daily (0.9 g/dose) (MSG group; n = 79) or a group that ingested NaCl thrice daily (0.26 g/dose) (Control group; n = 80). This study consisted of a 12-week intake period, followed by a 4-week follow-up period without the ingestion of MSG or NaCl. We performed physical examination, cognitive symptom tests (the Touch Panel-type Dementia Assessment Scale (TDAS) and Gottfries–Bråne–Steen Scale (GBSS)), palatability and behaviour questionnaires, and blood tests before and after the intervention and after the follow-up period. There were no significant differences in the TDAS and GBSS total scores between the groups before and after the intervention. However, regarding the TDAS sub-items, “the accuracy of the order of a process” did not deteriorate in the MSG group compared with that observed in the Control group (p < 0.05). At the follow-up assessment, the TDAS total scores in the MSG group showed significant improvement compared with those reported in the Control group (p < 0.05). Furthermore, there was a correlation of changes from pre-intervention to post-intervention between the TDAS and enjoyment of the meal (r = −0.299, p = 0.049). Our results suggest that continued ingestion of MSG has an effect on cognitive function. Furthermore, the patients with improved questionnaires about palatability survey showed greater improvement in cognitive function.

Background. Mucosal healing (MH) decreases the relapse risk in patients with inflammatory bowel disease, but the role of dietary supplementation in this process