Amino Acid-deficient Diets Research Articles

Fatty liver of pregnancy and its relationship to tetracycline therapy

Abstract The clinical, laboratory and pathologic features of sixteen patients with liver of pregnancy are presented. Four of these patients survived. Twelve patients in this series were treated for acute pyelonephritis with large doses of tetracycline intravenously, but four who had not received tetracycline had hepatic lesions that were indistinguishable from those in patients with liver of pregnancy. Six nonpregnant women treated with tetracycline intravenously had similar changes in the liver. There was a high incidence of pathologic or functional involvement of the pancreas, kidneys and brain. Central nervous system changes are described, severe enough to be etiologically related to the stupor and coma noted in many patients with liver of pregnancy who had previously received tetracycline. The similarity in morphology of liver of pregnancy with that in experimental lesions produced by protein anabolism depressants, such as ethionine or essential amino acid deficient diets, is reiterated. Levels of nonesterified acids in the liver, although elevated above normal, are no greater than nonesterified acids in livers due to other causes. The possibility exists that the liver during pregnancy is more sensitive to agents that depress protein anabolism, such as the tetracyclines. The question is also raised as to whether or not pre-existing pyelonephritis may also be a predisposing factor in the production of liver of pregnancy. It is proposed that liver of pregnancy be referred to as fatty liver of pregnancy, idiopathic, or fatty liver of pregnancy, tetracycline associated.

Survival Time and Biochemical Changes in Chicks Fed Diets Lacking Different Essential Amino Acids

Preceding death, three stages were observed in young chicks fed purified amino acid diets, lacking one or more essential amino acids: (1) a rapid loss of weight; (2) a relatively long period of essentially stable weight; and (3) another period of rapid weight loss, followed by death. The loss of weight in the first period and the length of the second period varied with the missing amino acid. Median survival times in days for chicks fed diets lacking the following amino acids are: isoleucine, 18; valine, 19; both phenylalanine and tryrosine, 23; methionine, 26; arginine, 27; threonine, 27; leucine, 28; both methionine and cystine, 28; all essential amino acids, 28; phenylalanine, 34; the combination of valine, isoleucine and leucine, 34; all amino acids, 35; tryptophan, 36; lysine, 53; and histidine, 60. Explanations for these survival times can be categorized as follows: (1) chicks fed diets lacking either isoleucine or valine suffered a severe amino acid imbalance, rapidly affecting the free amino acid levels in tissues and causing early death; (2) chicks fed diets lacking either lysine or histidine survived longer, possibly because of drawing on body stores of peptides (carnosine) and proteins (hemoglobin) especially rich in these amino acids for synthesis of necessary proteins; and (3) chicks fed diets lacking the other essential amino acids, either singly or in combination, survived approximately the same length of time as chicks fed an amino acid-free diet, although the effect on body composition differed. Chicks fed the essential amino acid-deficient diets lost body fat much faster than those fed the amino acid-free diet. All chicks had near-normal feather development and considerable skeletal growth at the expense of muscle tissue. Except for some chicks fed threonine-free diets, all chicks surviving past the median death time which were re-fed normal, complete diets had a rapid weight gain. The only lesion observed was a varied incidence of folded tongue.

Response of liver enzyme and other proteins to amino acid deficient diets.

Summary1. Histidine-deficient diet can completely restore xanthine oxidase activity to livers of rats previously depleted of such activity by a non-protein diet; methionine-free and lysine-free diets partially restore such activity with the lysine-free diet the least active in this respect. 2. Liver succinic oxidase activity can be similarly restored by histidine-and methionine-free rations but only partially restored by a lysine-free ration. 3. Liver choline oxidase activity of protein-depleted rats can be restored partially and to about the same extent by the 3 amino acid-deficient diets studied. 4. Liver nitrogen concentration follows approximately the same pattern as succinic oxidase in these studies. 5. The enzymatic responses to a non-protein diet followed by single amino acid-deficient diets have been compared to responses observed in earlier studies under conditions of initial single amino acid-deficient diets.

Studies on the Response of Liver Xanthine Oxidase to Dietary Protein in Weanling Rats

Several studies have been carried out in this laboratory relating the xanthine oxidase activity in the liver of adult rats to the quality of dietary protein (Litwack et al., '52, '53c). The behavior of this enzyme toward fasting and pro tein and amino acid-deficient diets (Miller, '48; Seif ter et al., '48; Litwack et al., '50; Williams and Elvehjem, '49, '50; Williams, DentA3n and Elvehjem, '49) has been exten sively studied, as have the effects of non-specific ammonium nitrogen sources on the enzyme activity (Litwack, Williams and Elvehjem, '53b). In some of our previous work using adult animals (Lit wack et al., '52, !53c) we have described a method for evalu ating the quality of dietary protein, using the response in liver xanthine oxidase activity as the criterion. We have also tested the quality of various protein preparations, using this method. After studying the deficient protein, gliadin, and supplementation of this protein with amino acids, it was concluded that the enzyme response was very sensitive to

OCULAR INVOLVEMENT IN RATS ON DIETS DEFICIENT IN AMINO ACIDS

OCULAR involvement and cataractous changes in the lens have been reported under a great number of experimental conditions (tetany; diabetes, including galactose and xylose cataract; thallium intoxication; riboflavin deficiency) and clinically in association with various cutaneous diseases, as well as with mongolism and myotonia. 1 More recently, blindness with opacities of the lens was described by Curtis and associates, 2 and cataractous changes in the lens with vascularization of the cornea were reported by Totter and Day, 3 Albanese and Buschke 4 and Buschke 5 in rats on tryptophan-deficient diets. During the past four years we have been studying the effects of various amino acid-deficient diets on the growth, development, morphology of various body tissues and organs, endocrine glands and nervous system in rats. Up to the present we have observed ocular involvement with diets deficient in tryptophan and valine. In rats on a tryptophan-deficient diet we were able to