The intestinal absorption of riboflavin was studied using radioactive riboflavin and its analogues 8-demethylriboflavin, 3-methyl-riboflavin, 5'-deoxyriboflavin, 2'-deoxyriboflavin, 7, 8-dimethyl-10-hydroxyethylisoalloxazine, lumiflavin, lumichrome, and riboflavin-5'-monosulfate, which were synthesized with high specific radioactivity. A specific absorption of riboflavin at dietary concentrations was confirmed using an in situ circulation system. The relation between the chemical structure of flavins and the absorption mechanism was studied using this system. The 8-demethylriboflavin, an analogue modified at benzene moiety of the isoalloxazine ring, was absorbed in a similar way to riboflavin, by dual kinetics: by a process specific for riboflavin at dietary concentrations and by simple diffusion (nonspecific absorption) pre-dominating at higher concentrations (over 100μM). However, 3-methylri-boflavin and analogues modified at the ribityl group, including 5'-de-oxyriboflavin, were absorbed only via simple diffusion even at dietary concentrations. Many flavins examined, except for 3-isobutylriboflavin, 3-carboxymethylriboflavin, lumichrome, and riboflavin-5'-monosulfate, in-terfered with the specific absorption of riboflavin. It was concluded from these results that one of the specific absorption processes for riboflavin is a phosphorylation-dephosphorylation process. Four water-soluble vitamins did not interfere with the specific absorption of riboflavin, indicating that these vitamins do not share a common specific absorption pathway with riboflavin.
Metabolic changes in lipids, ascorbic acid, and hepatic microsomal cytochrome P-450 by feeding polychlorinated biphenyls (PCB) were investigated in streptozotocin-induced diabetic rats. Strep-tozotocin (STZ, 60mg/kg body weight) was injected in Wistar male rats intraperitoneally. Diabetic and non-diabetic rats were fed ad libitum a 20% casein-based control diet or a PCB-containing diet (200 mg/kg diet) for 9 days. Body weight decreased significantly in STZ-induced diabetic rats with or without PCB (groups PD and D, respectively). In rats of group D, urinary ascorbic acid excretion was 15 times higher than that in non-diabetic rats fed a control diet (group C). Dietary PCB caused 30-fold higher urinary ascorbic acid excretion in non-diabetic rats (group P) than that in group C. In group PD, urinary ascorbic acid was nearly 60 times higher than that in group C. Ascorbic acid in liver and kidney was significantly lower in group D than in group C, and it was significantly lower in group PD than in group P. Liver microsomal cytochrome P-450 and b5 were both increased by dietary PCB in group P. Addition increase in these enzymes was observed in diabetic rats by PCB. Serum total cholesterol was 1.8 times higher in group P than in group C. Further increase in serum total cholesterol was observed in group PD. These data suggested that metabolic changes in lipids and ascorbic acid induced by the dietary xenobiotic were magnified in STZ-induced diabetic rats.
Nutritional status of vitamin E was assessed in very low birth weight infants of less than 1, 500g, with respect to changes in plasma and red blood cell (RBC) tocopherol concentrations. The forty infants examined were divided into two groups in terms of their birth weight: group A, less than 1, 000g; and group B, 1, 000-1, 500g. Immediately after birth, plasma tocopherol level was 335±101 μg/dl in group A and 316±103 μg/dl in group B, while RBC tocopherol was 187±48μg/dl and 231±72 μg/dl packed PBCs, in groups A and B, respectively. In two infants, RBC tocopherol concentrations were less than 115μg/dl, this level being reported as the lowest of the normal range. After birth, plasma and RBC tocopherol levels decreased markedly during 4 to 6 weeks of life especially in group A, while no decrease below normal range was docu-mented in RBC levels in group B. A fine granule preparation of tocoph-eryl nicotinate (20mg/kg/day) was administered in seven other infants, three in group A and four in group B. All three infants in group A showed no elevation of plasma and RBC tocopherol levels during the first 4 or 5 weeks of the administration, but a marked elevation thereafter. In three of the four infants in group B, an elevation of plasma and RBC tocopherol concentrations was documented after 2 weeks of the adminis-tration. The above findings indicate that no deficiency exists even in very low birth weight infants immediately after birth, while the deficiency may develop after birth, due to a poor ability to absorb fat.
We previously found that hepatic lipogenic enzyme in-duction, fatty acid synthesis, and triglyceride level were markedly lower in rats fed soybean protein than in those fed casein (Iritani et al. (1986): J. Nutr., 116: 190). After labeling triglycerides with tritiated water, the effects of dietary protein on the triglyceride degradation have been investigated. After the injection of tritiated water into rats, the radioactivities of fatty acids and triglycerides reached a plateau in 1-2 days and were markedly lower in the soybean protein group than in the casein group. The decreasing rates of triglyceride radioactivities were similar between the casein and soybean protein groups. The enzyme activities in glycerolipid synthesis were similar between the groups. Therefore, the lowering effects of soybean protein on triglyceride levels appear to be ascribed to triglyceride synthesis (due to fatty acid synthesis) rather than to the degradation.
Obesity was induced in neonatal mice by subcutaneous injections of monosodium glutamate (MSG) at an early neonatal stage. The process of adipocyte formation was studied comparatively in the developing epididymal adipose tissue of the MSG-treated mice and in normal mice during the period from the 6th to the 100th postnatal day. Tritiated thymidine autoradiographic studies showed that cell proliferation activity was the highest on the 6th postnatal day both in the MSG-treated and the control mice. In normal mice, however, cell proliferation took place less frequently after 6 days and had almost ceased after 49 days. In the obese mice, as evidenced by relatively high labeling indices, cell proliferation continued to occur even after 49 days. Ultimately there was no difference in the number of adipocytes counted by Hirsch's method in the MSG-treated and the control mice at the 100th postnatal day. The storage of fat droplets became more noticeable in obese mice than in normal mice after 35 days. The mean size of fat droplets of the obese mice was twice as large as that in normal mice on the 49th postnatal day. These results indicate that the MSG-induced obesity is of the hypertrophic type.
The changes in the intestinal glucose transport in strep-tozotocin-induced diabetic rats have been demonstrated with brush-border membrane vesicles. When Na+ -dependent D-glucose uptake and phlorizin binding activities were compared, both significantly increased either in the jejunum or ileum of diabetic rats compared with those of control. Kinetic studies showed the increases in the Vmax of glucose transport and the maximum binding of phlorizin (Bmax), whereas the Kt. and Kd remained unchanged, respectively. These results suggested that the increase in glucose transport in diabetic rat intestine was due to the increase in the number of the intact glucose transporters.
Since a lead acetate solution can remove most of the ultraviolet (UV) light in the range below 275nm which usually gives undesirable by-products in the photochemical conversion of ergosterol to vitamin D, it is useful as a filter solution for the reaction to obtain higher yield of vitamin D. When a 5% lead acetate solution was used as the filter, the yield of vitamin D was 20-25% higher than that without using filter solution.