Thiamin and vitamin B6 intakes and erythrocyte transketolase and aminotransferase activities in morbidly obese females before and after gastroplasty.

To assess the need for postoperative vitamin supplements, intakes and nutritional status of thiamin (B1) and vitamin B6 were studied in 18 female gastroplasty patients who received a placebo or different levels of supplemental vitamins. Postoperative erythrocyte transketolase basal (BA) and thiamin pyrophosphate-stimulated (SA) activities and activity coefficients (AC) correlated significantly with B1 intake. Despite a decrease in apotransketolase, low thiamin intakes were associated with increased AC values during the first 3 months. With return to low B1 intakes following repletion during month 4, the AC values remained normal with low total activities. Both alanine (EALT) and aspartate (EAST) aminotransferase apoenzyme levels declined and AC values increased significantly during the first 3 months. Although the EALT-indices were more sensitive to changes in B6 intake than the EAST-indices, the EASTBA and SA correlated most consistently with the intake. Postoperative dietary intakes of both vitamins were inadequate for maintenance of normal activities of these erythrocyte enzymes. Although B1 intake of greater than or equal to 1.0 mg/day was adequate for maintenance of normal thiamin status in most subjects of this study, supplementation with greater than or equal to 1.5 mg/day is prudent even though it may not prevent the early postoperative loss of apotransketolase. Vitamin B6 intake at the current recommended dietary allowance (1.6 mg) was not adequate to maintain coenzyme saturation of the erythrocyte aminotransferases. Marginal intake of other nutrients may have affected the utilization of both thiamin and vitamin B6.

Riboflavin intakes and status of morbidly obese females during the first postoperative year following gastroplasty.

Eighteen women participated in a prospective study to assess the need for supplemental riboflavin after gastroplasty. Three groups of five patients received either a placebo or 0.6 or 1.2 mg riboflavin daily for up to 12 months, except during months 4 and 7 when all participants were given a "one-a-day" supplement containing 1.7 mg riboflavin. Dietary intakes of riboflavin decreased from 1.43 +/- 0.17 mg before the operation to 0.70 +/- 0.07 mg at 3 months, and then increased to 1.02 +/- 0.17 mg by 6 months. Even at 12 months, only 33% of the subjects had dietary intakes greater than or equal to 1.2 mg. All those with total intakes less than or equal to 1.7 mg at 3 months had impaired riboflavin status, as indicated by an erythrocyte gluthatione reductase activity coefficient greater than 1.40 and an erythrocyte riboflavin concentration less than 372 nmol/L. In contrast, 62% of the same subjects had urinary riboflavin excretion in the acceptable range. Supplemental intake of 1.7 mg riboflavin appeared to prevent tissue depletion in all subjects.

Effect of energy restriction on riboflavin retention in normal and deficient tissues of the rat.

We investigated the effects of energy restriction on tissue riboflavin depletion and subsequent repletion of deficient tissues. Groups of male Sprague Dawley rats with average body weights between 268 and 275g were placed on energy-restricted diets consisting of 8g (31kcal or 130kJ) per day of a basal diet adequate in all other nutrients and either 12mg of riboflavin/kg or no added riboflavin. The ad libitum controls received additional energy as a mixture of sucrose, starch, and corn oil (10:3:1 by wt). No significant difference in the degree of riboflavin deficiency was detected between energy-restricted and ad libitum-fed rats as assessed by riboflavin concentrations in the liver and gastrocnemius and soleus muscles and by the erythrocyte glutathione reductase activity coefficient (EGRAC). Additional energy-restricted riboflavin-deficient rats were subsequently repleted by feeding either the supplemented basal diet with no additional energy or with ad libitum energy. Repletion of liver riboflavin concentration and reduction of the EGRAC values to control levels occurred regardless of energy intake. Muscle riboflavin concentrations were normal in the ad libitum-fed group but decreased in the energy-restricted rats despite 4 weeks of supplementation. The latter group had muscle riboflavin levels similar to those in the rats fed the riboflavin-deficient diet for 8 weeks. The results suggest that energy restriction impairs flavo-protein synthesis in muscle but not in the liver.

Plasma pyridoxal phosphate as indicator of vitamin B6 status in morbidly obese women after gastric restriction surgery.

Plasma pyridoxal phosphate (PLP) concentrations were determined in 15 morbidly obese women before and after gastric restriction surgery for weight reduction. The subjects received a daily vitamin-mineral supplement containing 2 or 3 mg of vitamin B6 for 9 days before the operation and either a placebo or a multivitamin supplement containing 0.4, 0.8 or 2 mg of vitamin B6 for 3 months postoperatively. During the fourth month, all subjects received 2 mg of supplemental vitamin B6 per day. Dietary intakes of the vitamin were calculated from 3-day intake records kept by the subjects. Blood samples for PLP determination were obtained preoperatively and twice between weeks 4 and 8 and at 3 and 4 months postoperatively. The mean concentration of plasma PLP increased significantly from preoperation to 4 to 5 weeks postoperation and returned to the preoperative level by 6 to 8 weeks, with no further changes during the rest of the experimental period. There was no correlation between plasma PLP and either total or supplemental intakes of vitamin B6 at any of the time periods studied. Significant positive correlations were found between the preoperative and the first two postoperative plasma PLP levels (r = 0.93 and 0.67, p less than 0.001 and 0.005, respectively) and between the rate of weight loss and plasma PLP at 4-5 weeks and at 4 months postoperatively. Muscle PLP reserve may be mobilized during the early postoperative period and complicate the use of plasma PLP as a measure of vitamin B6 status.

Effect of exercise on riboflavin status of rats.

The effect of exercise on the riboflavin status of male rats was studied after 6 or 8 wk of treadmill running. Sedentary and exercised rats were pair fed diets marginal in riboflavin (2.0 or 2.5 mg/kg), and their tissue riboflavin concentrations and erythrocyte glutathione reductase activity coefficients (EGRAC) were compared. The rats exercised for 8 wk had similar body weights but significantly greater weights for heart, gastrocnemius and soleus muscles, less epididymal fat and more total muscle nitrogen and riboflavin than their sedentary controls. Similar changes were evident after 6 wk of exercise, but some were not statistically significant. The EGRAC values of both exercised and sedentary rats responded to changes in dietary riboflavin but were not different from each other. The specific activity of mitochondrial acyl-CoA dehydrogenase (per milligram protein) of the soleus muscle was unaffected by exercise; however, when expressed per gram of tissue or per muscle, the activities in exercised rats were 25% (P less than 0.05) and 60% (P less than 0.01) higher, respectively, than in sedentary rats. On the basis of the riboflavin-dependent parameters measured in this study, exercise did not increase the dietary riboflavin requirement of growing rats but did increase total riboflavin retention in gastrocnemius and soleus muscles.

Riboflavin status of rats fed two levels of protein during energy deprivation and subsequent repletion.

Adult male rats were fed either a low protein (LP) or moderate protein (MP) diet (0.6 and 1.8 g casein per rat per day, respectively) and 30 micrograms riboflavin (RF) while their energy intakes were progressively restricted to about 30% (26 kcal/day) of the predepletion ad libitum consumption. Total weight losses in 4 weeks averaged 17.3 +/- 0.6 and 12.5 +/- 0.7% from the initial body weights for the LP and MP groups, respectively, despite equal energy deprivation. Although liver riboflavin concentrations (micrograms/gram) were significantly higher in the energy-restricted groups than in either the predepletion or the ad libitum--fed control groups, total liver riboflavin remained at the predepletion level in both restricted groups. During energy deprivation, muscle riboflavin decreased significantly from the predepletion level and was not affected by protein intake. Subsequent repletion with 100 micrograms riboflavin/day and energy at the level voluntarily consumed by the LP group increased body and liver weights with both levels of protein, but liver riboflavin increased only in the MP group. Muscle riboflavin did not return to the predepletion level in either restricted group. Erythrocyte glutathione reductase activity coefficients remained normal for all groups during the depletion-repletion cycle.

Effect of riboflavin status on acetaminophen toxicity in the rat.

The effect of riboflavin status on acetaminophen hepatotoxicity was determined in the rat. Groups of rats were fed one of the following diets: "riboflavin-free" (RFF), low riboflavin (LRF), high riboflavin (HRF), or high riboflavin pair-fed (HRF pair-fed) with RFF group. After riboflavin deficiency was established by determining erythrocyte glutathione reductase activity coefficient, rats in all groups were administered a toxic dose of acetaminophen (1 g/kg body weight) orally. Their controls were given the vehicle alone. All animals were killed 24 h later and hepatotoxicity was assessed by the elevation of serum transaminases and by a necrotic score based on histological examination. The RFF diet induced biochemical riboflavin deficiency, decreased food intake and body weight gain, and was associated with almost complete protection against acetaminophen toxicity. Rats on the LRF diet, with less severe riboflavin deficiency and no significant change in weight gain, showed some necrosis, but it was much less than in the HRF ad libitum-fed rats. The HRF pair-fed rats with no biochemical riboflavin deficiency but with considerable growth retardation also showed very little hepatic necrosis. Our results suggest that riboflavin deficiency protects rats against acetaminophen toxicity but it is confounded by decreased food consumption and body weight.

Growth and riboflavin status of rats fed different levels of protein and riboflavin.

The relationship between riboflavin and protein utilization was studied in 5-week-old male Sprague-Dawley rats, by using a factorial design with three levels of riboflavin (8, 16 and 24 microgram per rat per day) and protein (1.0, 1.6 and 2.2 g casein per rat per day) in a 9-week experiment. With the lowest level of casein, protein intake was growth limiting, and the level of riboflavin intake had no effect on either weight gain or liver nitrogen retention. With the two higher levels of casein, both weight gain and liver nitrogen retention increased with riboflavin intake, but 24 micrograms riboflavin per day was inadequate for maximal utilization of nitrogen from 2.2 g casein. Neither protein nor riboflavin intake affected the concentration of liver nitrogen per gram of fresh tissue. Increasing the protein intake from 1.0 to 1.6 g increased riboflavin retention in the liver, but additional protein had no further effect. Liver and muscle (gastrocnemius) riboflavin concentrations, as micrograms per gram wet tissue, increased with riboflavin intake. At the two higher intakes of riboflavin, tissue riboflavin levels decreased and the erythrocyte glutathione reductase activity coefficients (EGR-AC) increased with protein intake. These findings are consistent with the view that the effect of protein on riboflavin requirement is related to the rate of growth and not to protein intake, per se.

Lecithin supplementation in healthy volunteers: effect on cholesterol esterification and plasma, and bile lipids.

Plasma and bile lipids and in vitro cholesterol esterifying activity of plasma (mg CE/dl/6 h) were determined in healthy volunteers who supplemented their regular diets with 7.5 g doses of soya lecithin three times daily for a 4-week period. Lecithin ingestion by the 4 male and 6 female subjects did not produce any significant changes either in total plasma cholesterol (TC) level or cholesterol esterification. A small but significant reduction was observed in the plasma triglyceride (TG) and total phospholipid (TPL) levels after supplementation. The molar percent of bile acids (BA), TC and TPL as well as the lithogenic index (LI = TC/BA + TPL) in both hepatic and gallbladder bile were also unaltered by 4 weeks of lecithin supplementation. In vitro cholesterol esterification was found linearly related to plasma-free cholesterol (r = 0.60, p less than 0.01) cholesterol ester (r = 0.50, p less than 0.05), total phospholipid (r = 0.50, p less than 0.05), lecithin (r = 0.45, p less than 0.05), and triglyceride (r = 0.57, p less than 0.025) levels.