The effects of vitamin A deficiency, which results in a substantial decrease in the level of serum retinol binding protein, on the existent state of serum thyroxine and thyroid function were examined. In the vitamin A-deficient rats, the thyroid weight increased and the level of serum thyroxine decreased to one half that of the control rats. Normal thyroid weight and serum thyroxine levels were recovered by the replenishment of retinyl palmitate in the vitamin A-deficient rats. In addition, decreased hormone synthesis was observed in the thyroid glands of the vitamin A-deficient rats.
The determination of thyroxine distribution in rat serum proteins in vivo showed that thyroxine-binding prealbumin (TBPA) is a major thyroxine transport protein in the control rats, whereas in the deficient rats the amount of thyroxine bound to TBPA decreased and the thyroxine bound to thyroxine-binding globulin (TBG) increased significantly as compared with observations in control rats. These findings suggest that the existent state of serum thyroxine and thyroid function is affected by the serum level of vitamin A.

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The effect of nicotinic acid on the changes of rat brain cerebroside levels has been studied during brain development. There is a gradual increase in the concentration of cerebroside from 12 days of age to adult level at approximately 47 days of age. However, the concentration of cerebroside was significantly lower in brain of rat fed the nicotinic acid-deficient diet. Therefore, nicotinic acid may play an important role in cerebroside synthesis in brain of developing rat.

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Endogenous biosynthetic capacities for prostaglandin (PG)E₂, thromboxane (TX)B₂ (a stable degradation product of TXA₂) and 6 keto-PGF_1α (a stable degradation product of PGI₂) in the brainstem fractions of stroke-resistant spontaneously hypertensive rats (SHRSR) and control Wistar-Kyoto rats (WKR) were determined with novel methods and presented in an original report. In comparison with WKR, it is characteristically found that TXB₂ synthesis is increased in excess of threefold in the pons-medulla oblongata of SHRSR, while being decreased by 75% in the hypothalamic region of SHRSR (0.01<p<0.05). On the other hand, the biosynthesis of PGE2 is adaptively elevated in both hypothalamus and pons-medulla oblongata regions of each animal, although the PGI₂/PGE₂ ratio was lowered in both these regions of SHRSR.

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The effects of three vitamin B6 analogs were studied in young adult and weanling rats. The 2-ethyl analog was the most active. It produced higher growth rates, an average feed efficiency equal to the control and elevated liver glycogen levels. Xanthurenic acid excretion remained low with the 2-ethyl analog and pyridoxine in the diet and plasma amino acid concentration was low. Response to the 2-n-propyl analog was similar to that of a B6-deficient diet, with a large increase in xanthurenic acid excretion. Rats receiving the 2-isopropyl analog were intermediate between the ethyl group and B6-deficient animals in all parameters measured.
These in vivo results parallel those reported in the in vitro yeast pyridoxine dehydrogenase enzyme system. The ethyl pyridoxine analog was the most active of all the analogs in the yeast dehydrogenase system, in supporting growth and in maintaining normal xanthurenic acid excretion in the rat.

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Of a number of divalent cations investigated, Zn²⁺ strongly inhibited lactate production from glucose 6-phosphate in rat muscle cytosol fraction. The I₅₀ value for lactate production influenced by Zn²⁺ was 10μM and was increased to 200μM and 18μM by the addition of 10mM histidine and 10mM carnosine, respectively. The inhibitory effect of 50μM Zn²⁺ on lactate production was completely reversed by the addition of 1.2mM histidine and the apparent K_m was found to be 0.34mM.
The inhibitory site for Zn²⁺ was investigated by the estimation of glycolytic intermediates. It occurred at point between fructose 6phosphate and fructose 1, 6-bisphosphate. Purified rat muscle phosphofructokinase was inhibited by Zn²⁺. The I₅₀ values for Zn²⁺ were calculated to be 12, 5.5 and 1.5μM in the presence of 3, 0.3 and 0.06mM fructose 6-phosphate, respectively. The addition of histidine removed the inhibitory effect of Zn²⁺ on the glycolytic key enzyme. These studies indicate that in rat skeletal muscle the inhibitory effect of Zn²⁺ on lactate production might result from the inhibition of phosphofructokinase and that histidine could remove the effect.

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Lipogenesis in rat adipose tissue during postnatal development has been studied by measuring the incorporation of labeled glucose into lipid in fat cells and the activities of certain enzymes which participate in lipogenesis. It was found that: (1) Fatty acid synthesis from glucose is negligible in the suckling period. After weaning, it increases rapidly and reaches a plateau at the age of 10 weeks. (2) Insulin sensitivity is negligible in the suckling period. After weaning it rises and then declines. (3) Activities of ATP citrate lyase and acetyl CoA carboxylase are maintained at a low level in the suckling period. After weaning, these activities rise rapidly and then decline. (4) Weaning rats onto a high-fat diet showed decreases in glucose incorporation into fatty acids, insulin sensitivity, ATP citrate lyase activity and acetyl CoA carboxylase activity.

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Effects of anemia on serum total cholesterol and tri glyceride levels were studied in Sri Lanka. In subjects with hemoglobin (Hb) levels of less than 9.0g/100ml, there was a significant relationship between Hb and cholesterol levels (r=0.53). This relationship was not seen in subjects with Hb levels equal to, or greater than, 9.0g/100ml. Triglyceride levels were independent of Hb levels. Total cholesterol levels were elevated following an increase in Hb levels by transfusion and iron treatment. It was suggested that the concentration of red blood cells may affect cholesterol synthesis or mobilization from tissue to plasma.

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The nutritional value of N-acetyl-L-tryptophan (NALT) given intravenously was examined in unrestrained adult rats. They were given solutions of 4% Vuj pattern amino acids, 24.5% glucose, vitamins and electrolytes intravenously for 10 days. They were divided into three groups; one group was then injected intravenously with complete amino acid solution (T group), one with tryptophan-free amino acid solution (TF group) and one group with complete amino acid solution but with NALT instead of tryptophan (NALT).
The biological value of the NALT group was 49.6; this value corresponded to 90% of that of the T group. Excretion of injected amino acids totalled about 2.0 to 3.0% in this experiment. The effects of NALT on carcass composition, certain blood constituents and tryptophan pyrrolase activity in the liver were also examined.

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Conventional (CV) and germ-free (GF) mice were fed on a semi-synthetic diet containing graded levels of cellulose (0, 5, 15 and 30%), and thereafter the length and wet weight of intestine, the morphology of mid jejunum epithelium and the turnover of mid jejunum epithelial cells were determined. The following results were obtained.
Enlarged stomachs were observed in CV mice fed on a non-cellulose or 30% cellulose diet, but there were no differences found among the four dietary groups in GF mice.
On the other hand, no effect of intestinal bacteria was observed, at least with regard to caecum weight, since the responses of caecum wet weight to the graded cellulose intake in CV mice were similar to those in GF mice. The responses of intestine length to graded cellulose intake differed between CV and GF mice, indicating that intestinal bacteria may modify the length of intestine in some way. Marked differences were observed in the responses of villus length to graded levels of cellulose between CV and GF mice.
That is, in CV mice there was a gradual increase in villus length as cellulose content increased, whereas in GF mice there was a marked decrease in villus length.
In the CV mice, graded levels of dietary cellulose had no effect on the epithelial cell turnover. On the other hand, in the GF mice it was observed that the greater the amount of dietary cellulose, the faster the turnover rate becomes. As a result, dietary cellulose would enhance the turnover rates of jejunal epithelial cells only in the absence of intestinal bacteria.

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Increases in cytochrome P-450 and cytochrome b₅ and a decrease in NADPH-cytochrome c (P-450) reductase were generally brought about by feeding the riboflavin-deficient diet to young rats (50-120 g body weight) for 5 weeks, whereas no significant changes in these enzymes were observed with rats of 220 g body weight by feeding for 2 weeks. Amounts of lipid peroxides in the serum or the liver tissue and microsomes increased significantly after feeding the deficient diet for 5 weeks, in comparison with the respective control rats. On the other hand, NADPH-dependent lipid peroxidation in the presence of ferric ion and pyrophosphate, assayed as malondialdehyde, was decreased drastically in the liver microsomes of all groups of riboflavin-deficient rats irrespective of the period or body weight of animals. Lipid peroxidation could be detected by addition of EDTA-ferric ion or ferricyanide to the incubation medium, though the formation of malondialdehyde was less than that expected by the activity of NADPH-cytochrome c reductase. NADPH-reduction of nitroblue tetrazolium with liver microsomes was decreased in riboflavin deficiency, and was almost able to be correlated with the activity of NADPH-cytochrome c reductase.
Following intraperitoneal injection of riboflavin into the deficient rats, NADPH-dependent lipid peroxidation in the presence of ferric ion and pyrophosphate recovered only to 10% of the control rates at 40 hr after the injection, when cytochrome P-450, cytochrome b₅ and NADPH-cytochrome c reductase levels were restored to those of their respective controls.
Activities of drug-metabolizing enzymes, aminopyrine demethylase and aniline hydroxylase were decreased by initiation of feeding from the weanling stage, but the activities changed only slightly by feeding from the 120g of body weight stage.

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