Several lines of evidence demonstrate the relationship between vitamin E deficiency and cognitive dysfunction in rodent models, but little is known about the underlying mechanisms. In this study, we found axonal injury in the hippocampal CA1 region of vitamin E-deficient and normal old mice using immunohistochemical assay. The number of cells in the hippocampal CA1 region of vitamin E-deficient mice and normal old mice was significantly lower than in normal young mice. It is well known that collapsin response mediator protein (CRMP)-2 plays a crucial role in the maintenance of axonal conditions. The expressions of CRMP-2 in the cerebral cortex and hippocampus of vitamin E-deficient mice were significantly lower than both the regions of normal ones. In normal old mice, the expression of CRMP-2 in the cerebral cortex was significantly lower than in the normal ones. In addition, the appearance of microtubule-associated protein (MAP)-light chain 3 (LC3), a major index of autophagy, was higher in the cerebral cortex and hippocampus of vitamin E-deficient mice than in normal young and old mice. These results indicate that axonal degeneration is induced in living tissues, but not cultured cells, and that changes in CRMP-2 and MAP-LC3 may underlie vitamin E-deficiency-related axonal degeneration.
The aim of the current study was to examine the efficiency of a free-living physical activity promotion (PAP) program following a diet modification program for fat loss. Fifty obese men, aged 51.4±7.0 y, received a 6-mo regimen consisting of 2 phases. Weekly 90-min free-living PAP sessions were provided for 3 mo immediately after a 3-mo diet modification phase. Fat mass (FM) was measured at baseline and at months 3 and 6 using dual energy X-ray absorptiometry. The time spent in moderate-vigorous physical activity (MVPA) was monitored by a validated single-axis accelerometer. The total energy intake of all participants was assessed at baseline and during weeks 9 and 10 of both the diet modification and PAP programs. The change (Δ) in FM was −1.4±1.9 kg (p<0.05) during the PAP program after the diet modification program (−4.3±2.9 kg, p<0.01). Although there was no significant relationship between ΔFM and ΔMVPA during the PAP phase (p=0.11), MVPA was significantly increased during the PAP phase (+76.0±146.5 min/wk, p<0.01). However, a significant correlation was observed between energy intake/weight and MVPA during the PAP program (r=0.39). Our results suggest that the magnitude of expected FM loss induced by an increase in PA may be suppressed as a result of increased energy intake, even during a PAP program after a diet modification program.
This study was conducted to determine the anti-obesity effects of Zanthoxylumpiperitum DC fruit ethanol extract (ZPE) in 3T3-L1 adipocytes and obese mice fed a high-fat diet. We evaluated the influence of the addition of ZPE to a high-fat diet on body weight, adipose tissue weight, serum and hepatic lipids in C57BL/6 mice. In addition, adipogenic gene expression was determined by Western blot and real-time reverse transcription-PCR analysis. We assessed the effect of ZPE on 3T3-L1 preadipocyte differentiation. ZPE reduced weight gain, white adipose tissue mass, and serum triglyceride and cholesterol levels (p<0.05) in high-fat diet-fed C57BL/6 mice. ZPE decreased lipid accumulation and PPARγ, C/EBPα, SREBP-1, and FAS protein and mRNA levels in the liver. ZPE inhibited in vitro adipocyte differentiation in a dose-dependent manner and significantly attenuated adipogenic transcription factors, such as PPARγ, C/EBPα, and SREBP-1 in 3T3L1 cells. These findings suggest that Z. piperitum DC exerts an anti-obesity effect by inhibiting adipogenesis through the downregulation of genes involved in the adipogenesis pathway.
Vitamin A is beneficial in counteracting free radical damage, therefore the present study is designed to investigate the effect of vitamin A against isoproterenol-induced myocardial infarction in rats. Male Wistar rats were divided into three groups, namely a normal control group, an isoproterenol group (150 mg/kg, s.c.), and a vitamin A treatment (4,500 IU/kg/d, orally) group. Vitamin A-treated rats demonstrated significant reduction in ST-segment (p<0.001) and infarct sizes (p<0.05) when compared with the isoproterenol group of rats, suggesting that vitamin A markedly attenuated myocardial injury. Vitamin A treatment resulted in a significant decrease in the serum level of troponin I (p<0.001), creatinine kinase-MB (p<0.01), creatine kinase (p<0.05), lactate dehydrogenase (p<0.05), aspartate aminotransferase (p<0.01) and alanine aminotransferase (p<0.01). Vitamin A treatment resulted in a significant decrease in malondialdehyde (p<0.001), and significant increases were observed in reduced glutathione (p<0.01), superoxide dismutase (p<0.05) and catalase (p<0.001). Vitamin A treatment resulted in a significantly increased level of Na+-K+ ATPase (p<0.05) and Mg2+-ATPase (p<0.01) and a significant reduction of Ca2+ ATPase (p<0.01). Vitamin A treatment also demonstrated a significantly decreased level of C-reactive protein (p<0.05) and myeloperoxidase activity (p<0.01). In conclusion, vitamin A attenuated the myocardial infarction and prevention was shown via membrane stabilization, reduction in oxidative stress, and prevention of neutrophil infiltration.
Coffee has an anti-diabetic effect, specifically the amelioration of both hyperglycemia and insulin resistance, in KK-Ay mice, a type 2 diabetes animal model. To investigate coffee's effect on insulin signaling in liver, skeletal muscle, and adipose tissue (epididymal fat), we assayed the tyrosine phosphorylation of insulin receptor (IR) and serine phosphorylation of Akt. In Expt. 1, we assayed insulin signaling under nonfasting conditions in KK-Ay mice that ingested water or coffee for 4 wk. Coffee ingestion ameliorated the development of hyperglycemia but did not affect insulin signaling in liver or skeletal muscle under such conditions. In Expt. 2, we assayed insulin signaling under basal and insulin-stimulated conditions in KK-Ay mice that ingested water or coffee for 3 wk. The levels of tyrosine phosphorylation of insulin receptor in response to insulin injection in insulin-sensitive tissues were not different between mice that drank water and those that drank coffee. Coffee ingestion significantly increased the insulin-induced serine phosphorylation of Akt in liver and skeletal muscle, but not in epididymal fat, of KK-Ay mice. Our results also indicated that coffee ingestion may contribute to the improvement of insulin resistance and hyperglycemia in KK-Ay mice via the activation of Akt in insulin signaling in liver and skeletal muscle.
Ample evidence indicates that a high-protein/low-carbohydrate diet increases glucose energy expenditure and is beneficial in patients with type-2 diabetes mellitus (T2DM). The present study was designed to investigate the effects of L-tryptophan in T2DM. Blood glucose was measured by the glucose dehydrogenase assay and serum insulin was measured with ELISA in both normal and hereditary T2DM rats after oral glucose administration with or without L-D-tryptophan and tryptamine. The effect of tryptophan on glucose absorption was examined in the small intestine of rats using the everted-sac method. Glucose incorporation in adipocytes was assayed with [3H]-2-deoxy-D-glucose using a liquid scintillation counter. Indirect computer-regulated respiratory gas-assay calorimetry was applied to assay energy expenditure in rats. L-Tryptophan suppressed both serum glucose and insulin levels after oral glucose administration and inhibited glucose absorption from the intestine. Tryptamine, but not L-tryptophan, enhanced insulin-stimulated [3H]-glucose incorporation into differentiated adipocytes. L-Tryptophan increased glucose-associated energy expenditure in rats in vivo. L-Tryptophan-rich chow consumed from a young age preserved the secretion of insulin and delayed the progression of T2DM in hereditary diabetic rats. The results suggested that L-tryptophan suppresses the elevation of blood glucose and lessens the burden associated with insulin secretion from β-cells.
Resistant maltodextrin (RMD) is a soluble dietary fiber ingredient whose physiological functions are well recognized in Foods for Specified Health Use (FOSHU) for maintaining healthy intestinal regularity, blood glucose levels, and serum lipids. However, its efficacy on combined health risks—metabolic syndrome—was not studied yet. In this study the efficacy of RMD on humans with metabolic syndrome was investigated. A randomized double-blind placebo-controlled parallel-group trial was conducted. Thirty subjects with metabolic syndrome were randomly allocated into 2 groups and took either tea containing 9 g of RMD (treatment group) or placebo tea at three mealtimes daily for 12 wk. Blood was collected and body fat was scanned periodically. In the RMD treatment group, waist circumference, visceral fat area, fasting blood glucose, HOMA-R and serum triacylglycerol (TG) were significantly decreased compared to baseline, and significant time-by-treatment interaction was observed for waist circumference, visceral fat area, HOMA-R and serum TG (p=0.044, p=0.012, p=0.032, and p=0.049, respectively). The change ratio of visceral fat area showed negative statistical correlation with the baseline value (p=0.033), suggesting that efficacy of RMD was emphasized in the subjects having a larger visceral fat area. After the 12-wk RMD treatment, the total number of metabolic syndrome risk factors decreased to 20 from 32 with 2 subjects having no risks, while that of the placebo group decreased to 25 from 32. These findings suggest that continuous ingestion of RMD may improve the risk factors of metabolic syndrome by reducing visceral fat and improving glucose and lipid metabolism.
To determine the energy intake (EI) required to maintain body weight (equilibrium energy intake: EEI), we investigated the relationship between calculated energy intake and body weight changes in female subjects participating in 14 human balance studies (n=149) conducted at the National Institute of Health and Nutrition (Tokyo). In four and a half studies (n=43), sweat was collected from the arm to estimate loss of minerals through sweating during exercise on a bicycle ergometer; these subjects were classified in the exercise group (Ex G). In nine and a half experiments (n=106) subjects did not exercise, and were classified in the sedentary group (Sed G). The relationship between dietary energy intake (EI) and body weight (BW) changes (ΔBW) was analyzed and divided by four variables: body weight (BW), lean body mass (LBM), standard body weight (SBW), and body surface area (BSA). Equilibrium energy intake (EEI) and 95% confidence interval (CI) for EEI in Ex G were 34.3 and 32.8-35.9 kcal/kg BW/d, 32.0 and 30.8-33.1 kcal/kg SBW/d, 46.3 and 44.2-48.5 kcal/kg LBW/d, and 1,200 and 1,170-1,240 kcal/m2 BSA/d, respectively. EEI and 95% CI for EEI in Sed G were 34.5 and 33.9-35.1 kcal/kg BW/d, 31.4 and 30.9-32.0 kcal/kg SBW/d, 44.9 and 44.1-45.8 kcal/kg LBM/d, and 1,200 and 1,180-1,210 kcal/m2 BSA/d, respectively. EEIs obtained in this study are 3 to 5% higher than estimated energy requirement (EER) for Japanese. In five out of six analyses, EER in a population (female, 18-29 y, physical activity level: 1.50) was under 95% CI of EEI obtained in this study.
This study determined the vitamin B12 content of six wild edible mushrooms which are consumed by European vegetarians. Zero or trace levels (0.01-0.09 μg/100 g dry weight) of vitamin B12 were determined in porcini mushrooms (Boletus spp.), parasol mushrooms (Macrolepiota procera), oyster mushrooms (Pleurotus ostreatus), and black morels (Morchella conica). By contrast, black trumpet (Craterellus cornucopioides) and golden chanterelle (Cantharellus cibarius) mushrooms contained considerable levels (1.09-2.65 μg/100 g dry weight) of vitamin B12. To determine whether C. cornucopioides or C. cibarius contained vitamin B12 or other corrinoid compounds that are inactive in humans, we purified a corrinoid compound using an immunoaffinity column and identified it as vitamin B12 based on LC/ESI-MS/MS chromatograms.
Alkaline phosphatase (ALP) hydrolyzes a variety of monophosphate esters into phosphoric acid and alcohol at a high optimum pH (pH 8-10). Human ALPs are classified into four types: tissue-non specific (TNSALP, liver/bone/kidney), intestinal, placental, and germ cell types. Based on studies of hypophosphatasia (HPP), which is a systemic bone disease caused by the presence of either one or two pathologic mutations in ALPL that encodes TNSALP, TNSALP was suggested to be indispensable for skeletal mineralization. In this study, we explored the possibility that dietary nutrients contribute to regulate serum bone-specific ALP (BAP) activity. Serum biochemical parameters, such as serum ALP, BAP, osteocalcin, and fibroblast growth factor 23 (FGF23), were measured in healthy young subjects (n=193). Dietary nutrient intakes were measured based on 3-d food records before the day of blood examinations. The presence of a carrier of the deletion of T at nucleotide 1559 (c.1559delT), which has been reported to be the most frequent in Japanese HPP, was not detected in any subject. By the analysis of BAP activity and other biochemical parameters or dietary nutrient intakes, we obtained significant correlations between BAP activity and serum phosphorus (r=−0.165, p=0.022), calcium intake (mg/1,000 kcal/d) (r=−0.186, p=0.010), or phosphorus intake (mg/1,000 kcal/d) (r=−0.226, p=0.002). Further study on the regulation of BAP activity and calcium and/or phosphorus homeostasis will provide useful data for improving skeletal health.
To examine the responses of the levels of B6-vitamers in several tissues to the dietary level of pyridoxine (PN), mice were fed diets containing 0, 1, 7 (the recommended level) or 35 mg PN HCl/kg diet for 5 wk. Compared with the 0 mg PN HCl/kg diet, the 35 mg PN HCl/kg diet caused the highest elevation in the concentration of pyridoxal 5'-phosphate (PLP) in small intestine and epididymal adipose tissue, moderate elevation in colon, lung, spleen and stomach, slight elevation in brain, kidney and liver (p<0.05), and no elevation in heart and gastrocnemius muscle. In general, the alterations in PLP level in many tissues and serum were remarkable for diets between 1 mg and 7 mg PN HCl/kg diets. Compared to the 7 mg PN HCl/kg diet, the 35 mg PN HCl/kg diet further elevated the PLP level in adipose tissue, spleen and stomach (p<0.05). Dietary supplemental PN elevated the level of PN in small intestine and colon in a dose-dependent manner (p<0.05), but not in other tissues. There was a significant correlation between the PN and PLP levels in small intestine and colon (p<0.05), implying that PN absorbed from the diet can be at least in part metabolized to PLP within the absorptive intestinal cells. The results suggest that the responses of concentrations of B6-vitamers to dietary level of PN greatly differ among several tissues.