The investigation was carried out to clarify the effects of various dietary protein contents on vitamin A status of rats exposed to prolonged immobilization through suspension. A rat wearing a special jacket to which metal chains were attached, was suspended for 10 days as an analogy of simulated weightlessness. Five groups of suspended rats were fed on the diets containing various amounts of casein (5, 10, 20, 40 and 60, w/w%), while control group received the 20% casein diet. Through suspending animals, a decrease in body weight gain and increase in adrenal weights occurred. Serum albumin concentration of the suspended rats fed on the 10, 20, 40 and 60% diets were the same as that of the control rats. The suspended rats showed lowered serum retinol concentrations and elevated hepatic retinyl palmitate contents without noticeable differences between the diets. The hepatic retinol levels were not clearly affected. In the suspended rats, testicular levels of retinyl palmitate and retinol significantly decreased as compared with the control. These parameters' alterations did not relate to serum albumin concentration and were independent of dietary protein levels. The results suggest that stress state may cause suppression of releasing hepatic vitamin A, resulting in a lowered serum retinol concentration, being independent of nutritional status of protein.
Both the ascorbic acid (AsA) and erythorbic acid (ErA) absorption in the small intestine of guinea pigs were determined by the perfusion of the small intestine using isotonic phosphate buffer recycled in situ. The absorption rate of AsA in the small intestine of guinea pigs was higher than that of ErA; however, Km of AsA absorption was lower than that of ErA in normal guinea pigs. In AsA-deficient guinea pigs, the absorption rates of both AsA and ErA were higher than those in normal ones. The absorption of AsA and ErA in the small intestine of guinea pigs was inhibited by ouabain. Furthermore, AsA and ErA inhibited each other's absorption. Based on the results, the net amount of the absorbed ErA in the small intestine may be lower than that of AsA, and ErA absorption mechanism seemed to be similar to that of AsA. The absorption rate of both AsA and ErA in the small intestine of guinea pig might be dependent on the AsA level in the tissues.
Two types of retinoic acid-binding proteins, designated as epididymal retinoic acid-binding protein (ERABP) types A and B, have been purified to homogeneity from rat genital organs. ERABP types A and B had molecular weights of 19, 000 and 18, 500 and isoelectric points of 5.72 and 5.90, respectively. The absorption spectrum of ERABP complex with retinoic acid had two peaks at 277 and 354nm, and showed similar uncorrected fluorescence spectra to that of cellular retinoic acidbinding protein (CRABP). These ERABPs were identified as major androgen-dependent epididymal proteins by amino acid sequences analyses. Furthermore, immunohistochemical examinations revealed that the ERABPs exist in the epithelium of the proximal portion of the epididymis and in the lumen of epididymal canal and seminal tract leading from the epididymis. The existence of ERABP strongly suggests that retinoic acid might be involved in the maturation of spermatozoa.
The present study was undertaken to determine whether administration of adriamycin causes the depletion of riboflavin content. Rats received intraperitoneal injections of adriamycin (4mg per kg body weight) for 6 consecutive days. Urinary riboflavin excretion began to increase after 2 days of treatment with adriamycin. Erythrocyte FAD levels decreased gradually and plasma lipid peroxide contents increased markedly at the 6th day. The activity coefficient of erythrocyte glutathione reductase showed a significant increase before the decrease of flavin content and the elevation of lipid peroxide level. Therefore, the value of this coefficient obtained from erythrocyte appears to be a reliable index of riboflavin deficiency, particularly during the early stage.
Effect of hypothalamic lesions on regulation of body weight and fat cell dynamics in obese mice were examined during refeeding after prolonged food deprivation. Obese mice, which were treated with monosodium glutamate for 5 postnatal days and had ventromedial nuclear lesions in the hypothalamus, were used. When adult obese mice were given a glucose electrolyte solution for 20-40 days, the body weight dropped to about 45% of their pre-treatment weight. After reinstituted feeding of normal mouse food ad libitum, their body weight and adipose tissue weight returned to pre-starvation level. Tritiated thymidine autoradiography revealed that cell proliferation occurred in the early stages of refeeding and some fat cells were renewed in the epididymal adipose tissue. Fat cell renewal was found more active in the experimental group than in the control. Thereafter, fat cell size increased gradually via fat storage. These obese mice were found to have the capacity to regulate their body weight and adipose tissue not only through fat storage but also by increasing number of fat cells, in order to replace the cells which were lost during starvation. Therefore, ventromedial nuclear lesion in the hypothalamus does not influence the regulatory mechanism of adipose tissue during starvation and refeeding.
Five healthy young male subjects were given meals containing different levels of dietary fiber (DF) for one week each, and the effects on the fecal output, gastrointestinal transit time, frequency of evacuation, and apparent excretion rate of dietary fiber in feces were studied. The experiments were conducted twice by varying the subjects and the DF levels. The following results were obtained. 1) With an increase in the intake of DF, feces increased significantly in both wet weight and volume. The fecal specific gravity did not show any clear-cut relation with the intake level of DF. 2) The gastrointestinal transit time tended to shorten in each DF period compared to the DF-free period. However, it did not shorten with an increase in the intake level of DF. 3) Frequency of evacuation tended to be high in any of the DF periods compared to the DF-free period. However, the differences in the intake level of DF produced no changes in the frequency. 4) The DF content in feces increased significantly with an increase in the intake of DF, indicating that the larger the fecal output, the larger the fecal DF content. The apparent mean excretion rate of DF in feces remained in the range of 60-75% throughout the two experimental phases. Residues in feces other than DF increased with an increase in the DF intake. 5) The results obtained here indicate that the DF intake of at least 20g per day produces 140-150g of fecal output which can be easily excreted daily by a normal adult person.
Necessity of dietary vitamin B6 to the biopotency of sele-nium (Se) for the levels of Se and glutathione peroxidase (GSH-Px) in tissues was investigated. Male Wistar 12-week-old rats were fed a vitamin B6-Se-deficient basal diet for 3 week, and then the rats were divided into 6 groups. One group was fed the basal diet, the others were fed the diet supplemented with 250 1cg vitamin B6/100g as pyridoxine⋅ HCl, or 0.25mg Se/kg as Na2SeO3 (SeL) or DL-selenomethionine (Se-Met), or both (SeL+B6 or Se-Met+B6) for 10 week. The levels of Se and GSH-Px in erythrocytes and muscle were significantly higher in vitamin B6-supple-mented groups than in vitamin B6-deficient groups. There was little effect of this vitamin deficiency on Se level in liver of rats fed SeL; however, a higher Se level in liver was observed in vitamin B6-deficient rats fed Se-Met than in the corresponding B6-supplemented rats. A significant decrease of GSH-Px activity in liver was found in vitamin B6-deficient animals fed Se-Met compared with vitamin B6-supplemented animals, whereas no significant decrease was observed in those fed SeL. These results suggest that this vitamin is involved in the transport and deliver-ance of Se in plasma to the other tissues and the incorporation of Se from Se-Met to GSH-Px in liver.
The effect of dietary protein on pyrimidine-metabolizing enzymes was studied in the rat. The activities of dihydropyrimidine dehydrogenase and β-ureidopropionase in the livers of rats fed a protein-free diet were significantly decreased, while the activity of dihydropyrim-idinase was unaffected. Protein deficiency (5%) also decreased the activity of β-ureidopropionase. On the other hand, a high-protein diet (60%) increased the level of β-ureidopropionase. The activities of β-alanine-oxoglutarate aminotransferase (aminobutyrate aminotransferase) and D-3-aminoisobutyrate-pyruvate aminotransferase ((R )-3-amino-2-methylpropionate-pyruvate aminotransferase), which are present in mi-tochondria, depended on the amount of protein in the diet. Ammonium ions supplemented in the diet and given by injection did not affect the activities of rat liver pyrimidine-metabolizing enzymes (dihydropyrimi-dine dehydrogenase, dihydropyrimidinase, β-ureidopropionase, β-alanine-oxoglutarate aminotransferase and D-3-aminoisobutyrate-pyruvate ami-notransferase). Dietary uridine resulted in the accumulation of uracil in the liver, but did not affect the activities of pyrimidine-metabolizing enzymes.
Six healthy male subjects were given a single oral dose of 0.4g of maltitol per kg body weight containing [U-14C]-maltitol (50μCi) and their breath, urine, feces and blood were collected at appropriate intervals for 48h to measure the recovery of administered radioactivity. Further, to measure breath hydrogen, 15 healthy male subjects ingested 30g of maltitol and samples of their breath were collected for a 10-h period. The expired 14C02 showed a wide peak about 3 h after ingestion and 56% of the administered radioactivity was recovered in 48 h. An additional 0.2% of administered radioactivity was recovered as expired 14CH4, 2.6% in urine and 14.3% in feces, respectively. The obvious increase of breath hydrogen was detected at 1 h after maltitol ingestion and then a big peak at 3.5h, whereas maltose ingestion did not increase breath hydrogen. Both excretion profiles of breath 14C02 and hydrogen coincided well. These results demonstrate that a greater part of ingested maltitol is fermented by intestinal microbes than is hydrolyzed by diges-tive enzymes. Although maltitol is catabolized to carbon dioxide via intestinal microbes, the available energy is much lower than that of digestible sugars such as sucrose.