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The requirement for vitamin E is closely related to the dietary intake of polyunsaturated fatty acids (PUFA). By the protective mechanism to prevent PUFA from being peroxidized, vitamin E is metabolically consumed. In addition, PUFA impair the intestinal absorption of vitamin E. Therefore PUFA generate an additional vitamin E requirement on the order of 0.6, 0.9, 1.2, 1.5, and 1.8 mg vitamin E (RRR-alpha-tocopherol-equivalents), respectively, for 1 g of dienoic, trienoic, tetraenoic, pentaenoic, and hexaenoic acid. For this reason, the gross vitamin E content of food containing PUFA does not allow an evaluation of this food as a source of vitamin E. A suitable measure is the net vitamin E content, i.e., gross vitamin E minus the amount needed for PUFA protection. Therefore, some food-stuffs generally considered as vitamin-E sources, as concluded from their gross vitamin E content, cause in reality a vitamin E deficiency if not sufficiently compensated by other vitamin E supplying food constituents. Examples of the net vitamin E content of some fats and oils, fish and nuts are shown. Consequences for food composition data and food labeling and the problem of meeting the vitamin-E requirements are discussed.

Michaelis-constants and enzyme activities for dehydrogenation and transamination of the three branched chain alpha-keto acids in liver, kidney, skeletal muscle, and brain of rats are reported. After oral load only 11-22% of the keto acids pass the liver unchanged. Blood levels in pharmacokinetic and absorption studies are related to the Michaelis-constants. At the low keto-acid concentrations after oral application, dehydrogenation in the non-hepatic tissues is supposed to prevail over transamination. Data on feed efficiency of branched chain alpha-keto acids reported in the literature support this view. The chance for transamination is better after intravenous administration. The transferability of our data to humans, and various factors influencing the efficiency of branched chain alpha-keto acids are discussed in connection with data reported in the literature.

The uptake and chemical identification of 14C-retinyl acetate in the inner ear of the guinea-pig after oral administration is reported. For methodological reasons the experiment was carried out in vitamin A-deficient guinea-pigs. In the sensory tissues a time-dependent distribution was found similar to that in other organs. The chemical identification shows that the orally administered labeled retinyl acetate can be detected as retinyl palmitate in the membranous structures of the inner ear. This may be an indication for the ability of the inner ear tissues to esterize and probably store the transport form of vitamin A, retinol.

To estimate the role of vitamin A on ciliated cells we investigated whether ciliated cells undergo any alteration during vitamin A deficiency. The epithelia examined include the ciliated cells of the respiratory tract and the ciliated sensory cells of the inner ear, the tongue, and the olfactory cells. This part of the paper will describe the ciliated epithelium of the tracheobronchial tract and its relation to vitamin A status. During vitamin A deficiency a partial loss of ciliae can be observed before any squamous metaplasia (which usually occurs during longer lasting vitamin A deficiency) develops. The scanning electron microscopic data illustrate the altered surface of the epithelium during vitamin A deficiency better than transmission electron microscopy.

After a 5-day preoperative preparing period, 24 metabolically healthy patients, who had to undergo gastric resection, were fed postoperatively by hypocaloric total parenteral nutrition for a 5-day period. Group I, n = 13; received 0.11 g Xylitol/kg BW . h; Group II, n = 11, received 0.11 g Glucose/kg BW . h. Both groups received 1.71 g L-crystalline amino acids/kg BW . day. During the whole postoperative period, group II had significantly higher serum glucose and insulin levels. Due to the high postoperative insulin concentration in group II, free fatty acids, acetoacetate, beta-hydroxybutyrate and branched chained amino acids were significantly lower. The augmented release of muscle amino acids and the covering of a part of the energy expenditure by increased fatty acid oxidation in group I led to a higher postoperative synthesis rate of visceral proteins. From postoperative day 3 on transferrin and from postoperative day 6 on albumin and total protein were significantly higher in group I. This study could demonstrate that due to its special role in the intermediary metabolism during the postoperative period xylitol leads to a significantly higher regeneration rate of visceral proteins compared to glucose during total parenteral nutrition.

As demonstrated in the literature on vitamin A metabolism and homeostasis of retinol in serum, the concentration of retinol in serum is regulated very exactly if the liver stores are within the physiological range (20-300 micrograms/g liver). Therefore, the serum level indicates the status of vitamin A storage only if there is an extreme depletion or overconsumption of vitamin A. At marginal depletion, however, there is damage to peripheral tissue before changes in the vitamin A level in serum occur. At the beginning of hypervitaminosis A, changes in the level of vitamin A in serum also occur later. Therefore, the determination of vitamin A in serum gives no information on the adequacy of liver reserves for judging the necessity of a substitution.

Presently 3-methylhistidine excretion is widely used for monitoring the metabolic status of patients during different kinds of clinical conditions. Aim of the study was to reconsider its predicative value on the basis of a larger collective of healthy persons and to find a standardization independent from sex. Therefore endogenous 3-methylhistidine release of 40 healthy adults (24 women and 16 men) was measured and related to body weight, body surface area, arm muscle circumference, and nitrogen and creatinine excretion. A positive correlation could be observed only for 3-methylhistidine and creatinine excretion and that to the same extent both for females and males. Assuming that the excreted 3-methylhistidine is mainly originating from muscle protein the calculated daily protein breakdown amounted for women 39.9 g and 68.1 g for men. No difference between females and males could be observed in the percentual turnover of myofibrillar protein which has been estimated with 0.90 and 0.98 respectively. We interpret our results saying that endogenous 3-methylhistidine excretion is a valuable indicator for muscle protein breakdown in humans with intact kidney function. For the assessment of muscle proteolysis by 3-methylhistidine excretion in heterogenous groups of patients it is recommended to use the 3-methylhistidine/creatinine ratio or the percental turnover of myofibrillar protein.