Background and Aims: Many investigations suggested that peptide nutrition had a clinical advantage for nitrogen absorption. Recently, the cDNA encoding the H⁺/peptide cotransporter PepT1 was cloned. However, the regulatory mechanism of PepT1 expression under malnourished conditions has not been elucidated. The aim of this study was to clarify regulatory mechanisms of PepT1 expression. Methods: Sprague-Dawley rats were starved for 4 days, semistarved (50% amount of control) for 10 days, or given total parenteral nutrition (TPN) for 10 days. Rats with free feeding were used as control. Among those groups, the changes of PepT1 mRNA level in the jejunal mucosa and PepT1 protein density at the brush-border membranes were examined by Northern blot and by Western blot analysis, respectively. Results: Both starvation and TPN treatment caused a significant decrease in mucosal weight by 41 and 50% respectively. PepT1 mRNA level increased to 179% in the starved group and also to 161 and 164% in the TPN and semistarved groups, respectively. In contrast, sodium-dependent glucose transporter 1 mRNA expression showed no significant change. PepT1 protein density showed similar changes with the mRNA. Conclusions: PepT1 gene expression was significantly enhanced under the malnourished conditions in spite of atrophic changes of intestinal mucosa.

The tomato saponin a-tomatine has been proposed to kill sensitive cells by binding to cell membranes followed by leakage of cell components. However, details of the modes of action of the compound on fungal cells are poorly understood. In the present study, mechanisms involved in a-tomatine-induced cell death of fungi were examined using a filamentous pathogenic fungus Fusarium oxysporum. a-Tomatine-induced cell death of F. oxysporum (TICDF) occurred only under aerobic conditions and was blocked by the mitochondrial F 0 F 1 -ATPase inhibitor oligomycin, the caspase inhibitor D-VAD-fmk, and protein synthesis inhibitor cycloheximide. Fungal cells exposed to a-tomatine showed TUNEL-positive nuclei, depolarization of transmembrane potential of mitochondria, and reactive oxygen species (ROS) accumulation. These results suggest that TICDF occurs through a programmed cell death process in which mitochondria play a pivotal role. Pharmacological studies using inhibitors suggest that a-tomatine activates phosphotyrosine kinase and monomeric G-protein signaling pathways leading to Ca 2+ elevation and ROS burst in F. oxysporum cells.

Elemental diet (ED) therapy has been established as primary therapy for Crohn's disease, and home enteral nutrition (HEN) has been reported to control relapse at a dose of more than 30kcal/kg of ideal body weight. However, a decrease in ED compliance with long-term use is becoming problem. We developed an n-3 fatty acid-rich diet and carried out nutritional education specifically for Crohn's disease patients using HEN to facilitate compliance and to improve their nutritional status. After the introduction of this n-3 rich diet, disease activity was not altered, and nutritional status, especially serum n-3 fatty acid levels, improved. The remission periods in patients with poor compliance seemed to be prolonged by the nutritional education. Thus, a n-3 rich diet in combination with nutritional education specific for Crohn's disease patients is very important for the in maintenance of high compliance and for maintaining nutritional balance.

These results suggested that TNBS enteritis might be useful as an IBD animal model and that MCT modulates intestinal inflammation and is less damaging than LCT.

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