Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
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After a chloroform intraperitoneal injection, lactate dehydrogenase, alanine aminotransferase and particularly aspartate aminotransferase serum activities are much more raised in deficient animals. Liver ornithine decarboxylase (ODC) activity normally decreases in rats between the 4th. and the 7th. month after the weaning. In vitamin A deficient animals, basal values of the enzyme activity are lower and the decrease is deeper. But even at month 7, liver sustains a partial capacity of ODC recovery if retinol is fed during 15 days. Chloroform administration strongly enhances liver ODC activity in normal rats. In the deficiency, stimulation is lower in absolute value but relatively higher if referred to basal level. After retinol refeeding, chloroform stimulates enzyme activity to nearly normal values. Vitamin A deficiency impairs obviously liver ODC activity and its response to chloroform stimulation in rats, but the stroke is at least partially reversible in our conditions. Moreover, deficient animals maintain a non negligible capacity of ODC response under chloroform stimulation.
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PMID:[Toxicity of chloroform and vitamin A status in the rat]. 145 50

The link between dietary fats and cardiovascular diseases has necessitated a growing research interest in palm oil, the second largest consumed vegetable oil in the world. Palm oil, obtained from a tropical plant, Elaeis guineensis contains 50% saturated fatty acids, yet it does not promote atherosclerosis and arterial thrombosis. The saturated fatty acid to unsaturated fatty acid ratio of palm oil is close to unity and it contains a high amount of the antioxidants, beta-carotene, and vitamin E. Although palm oil-based diets induce a higher blood cholesterol level than do corn, soybean, safflower seed, and sunflower oils, the consumption of palm oil causes the endogenous cholesterol level to drop. This phenomenon seems to arise from the presence of the tocotrienols and the peculiar isomeric position of its fatty acids. The benefits of palm oil to health include reduction in risk of arterial thrombosis and atherosclerosis, inhibition of endogenous cholesterol biosynthesis, platelet aggregation, and reduction in blood pressure. Palm oil has been used in the fresh state and/or at various levels of oxidation. Oxidation is a result of processing the oil for various culinary purposes. However, a considerable amount of the commonly used palm oil is in the oxidized state, which poses potential dangers to the biochemical and physiological functions of the body. Unlike fresh palm oil, oxidized palm oil induces an adverse lipid profile, reproductive toxicity and toxicity of the kidney, lung, liver, and heart. This may be as a result of the generation of toxicants brought on by oxidation. In contrast to oxidized palm oil, red or refined palm oil at moderate levels in the diet of experimental animals promotes efficient utilization of nutrients, favorable body weight gains, induction of hepatic drug metabolizing enzymes, adequate hemoglobinization of red cells and improvement of immune function. Howerer, high palm oil levels in the diet induce toxicity to the liver as shown by loss of cellular radial architecture and cell size reductions which are corroborated by alanine transaminase to asparate transaminase ratios which are higher than unity. The consumtion of moderate amounts of palm oil and reduction in the level of oxidation may reduce the health risk believed to be associated with the consumption of palm oil. Red palm oil, by virtue of its beta-carotene content, may protect against vitamin A deficiency and certain forms of cancer.
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PMID:Palm oil: biochemical, physiological, nutritional, hematological, and toxicological aspects: a review. 1260 39

Chronic vitamin A deficiency induces a substantial delay in the rates of weight and height gain in both humans and experimental animals. This effect has been associated with an impaired nutrient metabolism and loss of body protein. Therefore, we analyzed the effect of vitamin A deficiency on endogenous proteolysis and nitrogen metabolism and its reversibility with all-trans retinoic acid (RA). Male weanling rats, housed in pairs, were pair-fed a vitamin A-deficient (VAD) or control diet until they were 60 d old. A group of deficient rats were further treated with daily intraperitoneal injections of all-trans RA for 10 d. Final body and tissue (i.e. liver and heart) weights were significantly lower and tissue:body weight ratios were similar in VAD rats and in controls. Conversely, the epididymal white fat:body weight ratio and the plasma concentrations of alanine aminotransferase and adiponectin were significantly higher in VAD rats, which also had hepatic macrovesicular lipid accumulations. Plasma and gastrocnemius muscle 3-methylhistidine, urine nitrogen, and plasma and urine urea concentrations were all significantly higher in the VAD group. The expression of the genes encoding urea cycle enzymes and their activities increased in VAD livers. These changes were partially reverted by all-trans RA. We propose that fuel partitioning in vitamin A deficiency may shift from fatty acids to protein catabolism as an energy source. Our results emphasize the importance of vitamin A on the energy balance control system and they provide an explanation for the role of vitamin A in protein turnover, development, and growth.
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PMID:Vitamin A deficiency increases protein catabolism and induces urea cycle enzymes in rats. 2018 84