Inevitable sodium loss under sodium restriction must not be construed as evidence for the estimated average requirement (EAR) for sodium (Na) in humans. We conducted human mineral balance studies to determine the EAR for some minerals (Na, K, Ca, Mg, P, Zn, Fe, Cu and Mn). Na concentration in arm sweat was low while those of calcium (Ca) and magnesium (Mg) were high, during relatively heavy bicycle-ergometer exercise under relatively low Na intake (100 mmol/d). This suggests that Na was released from the bone, the sole pool of Na, with Ca and Mg. Additionally, the negative balances of Ca and Mg was observed under a relatively low sodium intake (100 mmol/d) even with the sufficient supply and intake of Ca and Mg into human body. Finally, we found no correlation between the Na intake and the Na balance, while the Na-intake was correlated significantly to the balances of K, Ca and Mg. The Na intake necessary to keep the balances of Ca and Mg positive was calculated to be 68 mg/kg body weight/d. To learn the signs and symptoms of low sodium intake, we compared the results of a metabolic study in which subjects consumed diets with 6 g and 12 g salt/d respectively. The blood pressure decreased only with the 6 g/d group. Fecal moisture contents of the 6 g/d group were lower than for the 12 g/d group, suggesting the fecal Na was strongly reabsorbed with water when the dietary Na was insufficienct. Indiscriminate Na restriction may have adverse effects on health.

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The pathway of tryptophan (Trp)-nicotinamide is very important nutritionally because a vitamin nicotinamide is biosynthesized from an amino acid Trp. Until we started studying the factors that affect the Trp-nicotinamide conversion rate, little data existed. Data obtained from TDO (Trp 2,3-dioxygenase)-KO (knock-out) mice have revealed that mice can biosynthesize a necessary amount of nicotinamide from Trp by indoleamine 2,3-dioxygenase (IDO) even when TDO is lacking. It has also been shown that 3-hydroxyanthranilic acid is a key intermediate. Urine upper metabolites such as kynurenic acid and xanthurenic acid originate from non-hepatic tissues but not from the liver. Data obtained from quinolinic acid phosphoribosyltransferase (QPRT)-KO mice indicated that the Trp→quinolinic acid conversion ratio was 6%. Urine quinolinic acid levels and the conversion ratio of Trp to nicotinamide were the same between hetero and wild mice. These findings indicate that QPRT is not the rate-limiting enzyme in the conversion. Thus, the limiting factors in the conversion of Trp to nicotinamide are the amounts of 3-hydroxyanthranilic acid and quinolinic acid in the liver and the activity of liver 3-hydroxyanthranilic acid 3,4-dioxygenase. Studies on factors have shown that conversion of Trp to nicotinamide is increased by adequate intake of good quality protein, and adequate intake of unsaturated fatty acids and starch. However, conversion was decreased by deficient niacin, vitamin B₂, or vitamin B₆, excessive intake of protein, saturated fatty acids, or glucose and fructose, or intake of protein with low Trp content, and insufficient mineral intake.

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This study aimed to characterize serum 25-hydroxyvitamin D (25OH-D) values among Japanese children aged ≤48 mo. The study included 290 healthy infants and young children aged 0-48 mo (males/females=166/124) living in Shizuoka or Tokyo. The subjects were divided into three groups by age (Low Age: 0-5, Middle Age: 6-15, High Age: 16-48 mo). The vitamin D deficient state was defined as 25OH-D <12 ng/mL, the insufficient state as 12-20 ng/mL, and the sufficient state as >20 ng/mL. The seasonal variation of serum 25OH-D levels was also analyzed. The median serum 25OH-D levels in each group were: Low Age (n=50), 19 ng/mL; Middle Age (n=94), 30 ng/mL; and High Age (n=146), 30 ng/mL. The serum 25OH-D level was significantly lower in the Low Age group than in the other groups (p<0.01). Serum 25OH-D levels in summer and autumn (n=149) were significantly higher than in winter and spring (n=141) (33 vs. 25 ng/mL, p<0.01). In the Low Age group, there was a significant difference in serum 25OH-D levels between breast-fed infants (n=26) and formula-fed or mixed-fed infants (n=19) (12 vs. 32 ng/mL, p<0.01). However, there were no significant differences in 25OH-D levels between the two season classifications in either breast-fed or formula-fed and mixed-fed infants. Although clinical symptoms were not available, more than 75% of the breast-fed infants and 14.6% of infants and young children to whom food had been introduced were defined as having a vitamin D deficient or insufficient state. Breastfeeding seems one of the contributing factor to lower serum 25 OH-D levels among infants ≤5 mo of age.

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The study was conducted to understand better the mechanisms involved in liver changes when there is a combination of diet-induced obesity (DIO) and vitamin D deficiency (VDD). After 8 wk of feeding a control diet (C group) or a high-fat diet (HF), both with vitamin D, and counterpart groups without vitamin D (VitD− groups), we found in plasma: higher alanine aminotransferase, and aspartate aminotransferase in the VitD− groups, and more elevated total cholesterol in the HF group. Compared to their counterparts, HF and HF/VitD− showed hyperinsulinemia and higher hepatic triglycerides and steatosis. The protein expressions of markers linked with the vitamin D action were altered by VDD (vitamin D receptor VDR, 25-hydroxyvitamin D-24-hydroxylase CYP24A1, CYP27B1, and CYP2R1). The hepatic lipogenesis and fatty acid synthesis were enhanced by VDD (peroxisome proliferator-activated receptor PPARγ, sterol regulatory element-binding proteins SREBP1c, carbohydrate-responsive element-binding protein ChREBP, and fatty acid synthase FAS), but markers of beta-oxidation were reduced (PPARα and phosphoenolpyruvate carboxykinase PEPCK). In conclusion, the study provides convincing new evidence that there is an additive and adverse effect on the liver caused by the combination of VDD and DIO. The essence of these changes in the liver is in an increased lipogenesis and a reduced beta-oxidation, which predisposes to the accumulation of fat in the liver, accompanied by IR. The worsening of the pathogenesis of NAFLD may tilt to more severe stages of liver disease.

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Colon diseases can be affected by several factors such as gender difference and dietary supplemental vitamin B₆ (B₆). The nutritional status of B₆ is affected by gender difference, leading us to hypothesize that gender difference affects colon luminal environment, which is dependent on B₆ status. To investigate this hypothesis, we fed male and female rats a diet containing 1 mg, 7 mg, or 35 mg pyridoxine HCl/kg diet for 6 wk. We found significantly higher fecal mucin levels in female rats compared to those in male rats. Supplemental B₆ significantly increased fecal mucins and was particularly profound in the female rats. The abundances of cecal and fecal Akkermansia muciniphila (mucin degrader) were unaffected. The fecal mucin levels were significantly correlated with colonic free threonine and serine and with gene expression of colon MUC16, implying that the combined effect of gender and dietary B₆ on fecal mucins was mediated by the alteration in the levels of such amino acids and MUC16 expression. This study further showed the significant effects of gender difference on colonic free amino acids such as threonine, ornithine, asparagine/aspartate ratio, and glutamine/glutamate ratio, cecal and fecal Lactobacillus spp. levels, and colonic gene expressions of MUC16 and TLR8, the factors relating to colon health and diseases. Therefore, our findings suggest that gender difference and dietary B₆ may have an impact on colon diseases by modulating these parameters.

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Context: International interest in the Japanese diet has grown in recent years. Objective: The aim of this systematic review was to evaluate and organize the Japanese diet and dietary characteristics from an epidemiological perspective, mainly focusing on the nutritional and dietary elements. Data Sources: PubMed, Web of Science, Japan Medical Abstracts Society, JDream III, and CiNii databases were searched. Study Selection: The eligibility criteria included research with an epidemiological study design that was either cross-sectional, cohort, or case-control-based that defined the dietary patterns of the Japanese diet using dietary pattern analysis. A total of 39 research articles that described the Japanese diet were included. Data Extraction: The data that were extracted included the following: implementing country, location, study design, participant characteristics, key outcomes, methods used in the analysis of dietary patterns, and descriptions of the Japanese diet. Data Synthesis: As a result of the systematic review analyzing the descriptions of the Japanese diet from 39 selected articles, we were able to aggregate the descriptions into 16 categories from 33 factors. After performing a content analysis using a further aggregation of categories, we found that the top three applicable categories were soybeans/soybean-derived products, seafood, and vegetables; these were followed by rice and miso soup. Conclusion: The Japanese dietary content was found to be diverse based on an examination of epidemiological studies; however, we were able to aggregate the content into 16 categories. The Japanese diet is considered to be a dietary pattern that contains a combination of factors: the dietary staple, side dishes, and soup.

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Enzyme-treated asparagus extract (ETAS) is prepared from the lower, residual parts of asparagus, and some functionalities, such as anti-oxidative and neuroprotective activities, have been suggested. The purpose of the present study was to investigate the effects of ETAS on photoaging in the epidermal layer of the skin using cultured keratinocytes. Normal human epidermal keratinocytes were irradiated or left unirradiated with UV-B (10 mJ/cm²) and incubated with ETAS (0.5 or 2 mg/mL) or vehicle. After 3 or 13 h, molecular examinations were performed, and after 24 or 48 h, cell viabilities were determined by a CCK-8 assay. ETAS addition may induce keratinocyte migration and proliferation as well as apoptosis under molecular examination. These results suggest that ETAS might accelerate turnover of keratinocytes.

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Whey protein is associated with improvement of metabolic syndrome. This study aimed to evaluate effects of whey protein on atherosclerosis in ApoE^−/− mice. Male ApoE^−/− mice were fed with a high-fat/cholesterol diet (HFCD), or HFCD supplemented with 10% or 20% whey protein for 18 wk. At the end of experiment, serum lipid profiles and inflammatory cytokines were assayed. Livers were examined using HE staining and Oil Red O staining. Aortas were used for en face and cryosection analyses to observe aortic lesions. Western blotting analysis was used to assess relative protein expression of cholesterol metabolism in the liver and aorta. No significant differences were observed in body weight or food intake among the three groups. Liver examination demonstrated decreased lipid droplets and cholesterol content in the whey-protein-supplemented groups. En face lesion of the aorta revealed a 21.51% and 31.78% lesion reduction in the HFCD supplemented with 10% and 20% whey groups, respectively. Decreased lesion was also observed in cryosection analysis. Whey protein significantly increased the serum high-density lipoprotein cholesterol level by 46.43% and 67.86%. The 20% whey protein significantly decreased serum IL-6 (a proinflammatory cytokine) by 70.99% and increased serum IL-10 (an anti-inflammatory cytokine) by 83.35%. Whey protein potently decreased lipogenic enzymes (ACC and FAS) in the liver and NF-κB expression in the liver and aorta. Whey protein significantly increased protein expression of two major cholesterol transporters (ABCA1 and ABCG1) in the liver and aorta. Thus, chronic whey protein supplementation can improve HFCD-induced atherosclerosis in ApoE null mice by regulating circulating lipid and inflammatory cytokines and increasing expressions of ABCA1 and ABCG1.

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Cacao extract (CE) consumption has beneficial effects on human health, such as lowering the risk of obesity. However, the underlying molecular mechanism for the anti-obesity effect of CE remains incompletely understood. Here, we used a 50% aqueous alcohol extract of cacao mass, which is rich in methylxanthine derivatives (about 11%) and poor in flavan-3-ols (less than 1%), and assessed the suppression effects of this extract on adipocyte differentiation to investigate the anti-obesity mechanism. CE dose-dependently decreased fat accumulation in 3T3-L1 cells without affecting cell viability. CE also dose-dependently decreased the protein and gene expression levels of two adipogenesis-related transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding proteins (C/EBPs). Moreover, CE decreased protein expression levels of sterol regulatory element-binding protein 1 (SREBP1) and its downstream fatty acid synthase (FAS), which was accompanied by the retained localization of SREBP1 in the cytoplasm of 3T3-L1 cells. After ICR mice were fed a diet containing 1% CE for 1 wk, their white adipose tissue weight was lower, whereas their brown adipose tissue weight was higher compared with those of control animals. Additionally, the protein expression levels of PPARγ, C/EBPs, SREBP1, and FAS in the white adipose tissue of these mice were also lower than those in control animals. In contrast, diet supplementation with CE induced higher levels of phosphorylated AMP-activated protein kinase (AMPK) and its downstream acetyl-CoA carboxylase. In conclusion, methylxanthine derivative-rich CE decreases fat accumulation in adipocytes by downregulating the expression of the adipocyte differentiation master regulators through the activation of AMPK.

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This study was designed to determine whether there is a relationship between serum vitamin D levels and neurodevelopment and anthropometry in Chinese infants. A prospective cohort study with 160 women who gave birth to 160 healthy full-term infants and who were followed up for 6 mo was done. It included 80 pregnant women with vitamin D deficiency, and the other 80 pregnant women were enrolled matching the age and delivery method with a 25(OH)D level of more than 50 nmol/L. There was a signicant intergroup difference in length, weight or head circumference at birth (p<0.05). Meanwhile, there was a signicant intergroup difference in cognitive development and achievement at 6 mo (p<0.001). In multivariate analyses, maternal 25(OH)D levels less than 50 nmol/L were independently associated with a higher tendency for a low Bayley mental score (MDI) at 6 mo (OR=2.77, 95% CI: 1.44-5.35, p=0.002), as well as Bayley motor score (PDI) (OR=2.08, 95% CI: 1.07-4.04, p=0.032). Thus we observed that maternal vitamin D was associated with infant neurodevelopment and anthropometry.

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