Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic changes in rats fed a low protein diet were investigated during 3 weeks after weaning using lactalbumin (LP) as dietary protein source. The energy intake was higher and the weight gain lower in rats fed the low protein diet (6%, LP group) than in control rats (13% lactalbumin, C group). Low protein diet induced no changes in plasma glucose, free fatty acids, or triacylglycerol concentrations; however, plasma protein and urea concentrations were lower in LP than in C rats. Plasma free T3 was higher in LP than in C rats (+38%, day 21) and insulin progressively decreased during the experimental period (-56%, day 21) without change in glucagon. Liver glycogen and triacylglycerol concentrations (+40% and +180%, respectively, day 21), and cytosolic and mitochondrial redox states increased (+100% and +100%, day 21), and protein concentration was decreased (-15%, day 21). Pyruvate kinase (PK) and malic enzyme activities were higher in LP than in C rats throughout the experiment (+80% and +210%, respectively, day 21), and glucose-6-phosphate dehydrogenase (G6PDH) activity progressively decreased (-65%, day 21). Phosphoenolpyruvate carboxykinase (PEPCK) activity increased after 2 weeks on a LP diet (+35%, day 21) and fatty acid synthetase (FAS) activity increased only during the first week on the diet (+100%, day 7). Such hormonal and metabolic changes appeared to be associated with the development of a futile energy-wasting cycle between pyruvate and phosphoenolpyruvate.
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PMID:Metabolic changes in rats fed a low protein diet during post-weaning growth. 219 92

Apart from the classic distal renal tubular acidosis (RTA), the proximal RTA, and a few cases of distal RTA and renal bicarbonate wasting we know only 2 cases of infantile transient distal RTA with bicarbonate wasting. A 3 month-old male patient is admitted because of deficient suction, vomiting and dehydration. Despite a strong metabolic acidosis (pH 7,09, bicarbonate 8,6 mMol/l, chloride 110 meq/l) the urine is constantly alkaline; clinically the disease manifests itself in the form of an alkali-resistant RTA. Accompanying troubles such as inner ear deafness, G6PDH deficiency, hyperparathyroidism and vitamin D intoxication are to be excluded. A bicarbonate study carried out with care so as to prevent extracellular fluid expansion reveals the lack of excretion of titratable acid (-2.4 to +4.7 mueq/min/1.73 m2), an reduced excretion of ammonium (5 to 24.8 mueq/min/1.73 m2) with regard to GFR (42.4 ml/min/1.73 m2), and a constant loss of bicarbonate (FE HCO3- about 10%) covering most of the bicarbonate plasma concentration, which results in a constantly negative net acid excretion. Even with alkalosis there is no urine minus blood pCO2 increase. The renal excretion of gamma GT is significantly reduced. On substitution with high quantities of bicarbonate (10 meq/kg BW/day) the defect heals up at the age of 13 months. The pathogenesis of this disease is not quite clear, but is similar to that of the Lightwood infantile RTA. The acidification defect may be explained by a deficient hydrogen ions--secretion in the distal tubule; as for kinetics, it is not in the proximal tubule that the bicarbonate wasting occurs but it may be due to increased sodium delivery to the distal nephron.
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PMID:[Infantile transitory distal renal tubular acidosis with bicarbonate loss]. 286 14

Peroxisomes are ubiquitous subcellular organelles. They contain catalase and hydrogen peroxide-producing oxidases like fatty acyl-CoA oxidase. The latter enzyme is part of a special fatty acid beta-oxidation system which shortens long-chain fatty acids. The middle-chain acids formed are subsequently degraded by mitochondria. The capacity to remove very long fatty acids and trans-unsaturated acids found in hydrogenated oils is restricted to peroxisomes. Essentially, the peroxisomal beta-oxidation system is not constitutive but inducible by certain hypolipidaemic compounds which are distinguished by their capacity to lead to proliferation of peroxisomes. Thyroid hormones as well as prolonged exposure to cold and high fat diets, esp. with long-chain unsaturated fatty acids, also induce beta-oxidation and peroxisome proliferation. Two other beta-oxidative reactions namely the removal of the cholesterol side-chain, leading to the formation of bile acids, and the degradation of dicarboxylic acids as formed by omega-oxidation of fatty acids were shown to be connected with peroxisomes. Presumably also 3-hydroxy-3-methyl-glutaryl-CoA reductase, the key enzyme of cholesterol biosynthesis exists in a peroxisomal moiety. NADPH consumed in this reaction (and in the dihydroxyacetone phosphate pathway of glycerolipid synthesis) might be provided by glucose-6-phosphate dehydrogenase which was recently also found in peroxisomes. Peroxisomes are indispensable in forming saturated ether lipids and plasmalogens because alkyldihydroxyacetone phosphate synthase is a membrane enzyme exclusively located in peroxisomes. Certain other enzymes of the dihydroxyacetone phosphate pathway of glycerolipid synthesis are also found in peroxisomes. Because of the combination of oxidases like fatty acyl-CoA oxidase and catalase and the feasibility of reoxidising NADH within the peroxisomes the aerobic metabolism of peroxisomes is energy-wasting. Therefore they might be important in chemical thermogenesis and in the control of body weight. For all these reasons peroxisomes must be essential for human metabolism. This is further demonstrated by genetically caused disorders: Total absence of peroxisomes is connected with the fatal cerebro-hepatorenal Zellweger syndrome. Defective peroxisomal beta-oxidation is manifested in Schilder's disease (adrenoleukodystrophy) characterized by accumulation of very long fatty acids. Peroxisomes perform a number of complementary and auxiliary reactions in general cell metabolism, in particular the cata- and anabolism of certain lipids, and therefore deserve consideration in clinical chemistry.
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PMID:[The contribution of peroxisomes to lipid metabolism]. 371 95

In tropical areas of developing countries, the interactions among parasitic diseases such as soil-transmitted helminths (STHs) and malaria, and glucose-6-phosphate dehydrogenase deficiency (G6PDd), are complex. Here, we investigated their interactions and impact on anemia in school students residing in a conflict zone of northeast Myanmar. A cross-sectional survey was conducted between July and December 2015 in two schools located along the China-Myanmar border. Stool samples from the schoolchildren were analyzed for STH infections, whereas finger-prick blood samples were analyzed for G6PDd, hemoglobin concentrations, and Plasmodium infections. Among 988 enrolled children, Plasmodium vivax, Plasmodium falciparum, hookworm, Ascaris lumbricoides, and Trichuris trichiura infections occurred in 3.3%, 0.8%, 31.5%, 1.2%, and 0.3%, respectively. Glucose-6-phosphate dehydrogenase deficiency was present in 16.9% of the children, and there was a very high prevalence of anemia (73%). Anthropometric measures performed on all children showed that 50% of the children were stunted and 25% wasted. Moderate to severe anemia was associated with STH infections, stunting, and wasting. In addition, children had increasing odds of anemia with increasing burden of infections. This study revealed a high prevalence of G6PDd, STHs, and anemia in schools located in a conflict zone. In areas where malnutrition and STH infections are rampant, testing for both glucose-6-phosphate dehydrogenase and anemia should be considered before treating vivax malaria with 8-aminoquinolines.
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PMID:Associations among Soil-Transmitted Helminths, G6PD Deficiency and Asymptomatic Malaria Parasitemia, and Anemia in Schoolchildren from a Conflict Zone of Northeast Myanmar. 3204 53