Several beneficial health effects of green tea (Camellia sinensis) have been documented. These include anti-carcinogenic, anti-allergic, anti-hypertensive, anti-cardiovascular disease, and anti-hypercholesterolemic activities. The compounds responsible for these activities are a subgroup of polyphenols known as catechins. The major green tea catechins are (－)-epigallocatechin-3-gallate (EGCG) , (－)-epicatechin-3-gallate, (－)-epigallocatechin and (－)-epicatechin. Because EGCG is found only in tea from Camellia sinensis, EGCG is regarded as a characteristic constituent of green tea. EGCG is known to exhibit various biological and pharmacological properties. The 67-kDa laminin receptor (67LR) has been identified as a cell-surface EGCG receptor that confers EGCG responsiveness to many cells at physiological concentrations. 67LR has been shown to mediate the beneficial activities of this phytochemical, which include anti-cancer, anti-allergic, anti-inflammatory and insulin sensing modulation activities. MYPT1, eEF1A, protein phosphatase 2A, Akt, endothelial nitric oxide synthase, soluble guanylate cyclase, protein kinase Cδ, acid sphingomyelinase, sphingosine kinase 1 and cGMP are molecules known to be related to the bioregulatory effects of EGCG via 67LR. Some food factors potentiate the bioactivities of EGCG by modulating the EGCG-sensing pathway.

Magnesium (Mg) deficiency is an actual dietary problem in developed countries including Japan. We have studied mineral nutrition centered on Mg using laboratory animals and cultured cells. We evaluated Mg absorption from marine algae and drinking water, and the results indicated that the forms of soluble Mg and sojourn time of Mg in the digestive tract affected Mg absorption. Mg deficiency induced the appearance of mast cells in the liver, a phenomenon that has been linked to the pathogenesis of non-alcoholic fatty liver disease. Comprehensive and non-targeted analysis of metabolites clarified that Mg deficiency disturbs some aspects of metabolism in both the liver and hepatic cell models. Comprehensive and targeted analysis of metals indicated that Mg deficiency affected the hepatic concentration of 8 metals including molybdenum. Mg deficiency increased the hepatic zinc concentration through increased expression of the zinc transporter (Zip14) and metallothionein genes. Mg deficiency increased the hepatic iron concentration by the unresponsive expression of hepcidin gene as a result of BMP signal blunting. Activin B and interleukin-1β enhanced the expression of hepcidin, which is probably one aspect of the pathogenesis of inflammatory anemia.

We aimed to clarify the relationship between frailty and insufficient nutrient intake in older outpatients attending a frailty clinic, independent of energy intake. The subjects were 270 patients with a median age of 79 years who had no moderate or severe cognitive impairment, comorbidities requiring protein restriction, or physical dependency. Frailty was evaluated using the J-CHS criteria. Nutrient intake was assessed with a brief-type self-administered diet history questionnaire, and adjusted to the required energy intake for each individual. The criteria for sufficient intake of 22 nutrients were based on the Dietary Reference Intakes for Japanese. The association between frailty and insufficient nutrient intake was analyzed by the logistic regression model. The dependent variable was nutrient intake deficiency, the independent variable was frailty, and the covariates were age and BMI. We found that there was a significant association between frailty status and insufficient intake of zinc with an odds ratio (95% confidence interval) of 2.50 (1.23‐5.06) in women, but not in men. Our results indicate that paying attention to sufficient intake of zinc is an important part of nutritional therapy for frail older women.