Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study was conducted to investigate the effect of vitamin A, B1 and B6 deficiency on oxalate metabolism in rats. A significant hyperoxaluria was the common observation in all the three vitamin deficiencies (vitamin B6 greater than vitamin A greater than vitamin B1). The activities of hepatic glycolate oxidase and glycolate dehydrogenase were markedly enhanced in vitamin-A- and vitamin-B6-deficient rats. However, lactate dehydrogenase levels remained unaltered in these deficiencies as compared to their respective pair-fed controls. Vitamin B1 deficiency of 4 weeks' duration could augment the activity of glycolate oxidase only, with no alterations in the glycolate dehydrogenase and lactate dehydrogenase levels. Intestinal oxalate uptake studies revealed increased bio-availability of oxalate from the gut in vitamin-A- and vitamin-B6-deficient rats. Thus, the results suggest the relative contribution of both exogenous as well as endogenous oxalate in the process of calculogenesis under various nutritional stress conditions in rat.
 ...
PMID:Comparative studies on the effect of vitamin A, B1 and B6 deficiency on oxalate metabolism in male rats. 236 74

Male weanling rats were maintained on a thiamine-deficient diet for 4 weeks, and compared with ad libitum and pair-fed controls. Thiamine deficiency led to slow growth and finally a decrease in body weight. Liver and kidney weights of the deficient rats were low, but appropriate to the body weight. Thiamine deficiency also caused a significant decrease in erythrocyte transketolase levels. The decarboxylation of glyoxylate both via the glyoxylate oxidation cycle and alpha-ketoglutarate:glyoxylate (alpha-KG:GA) carboligase was significantly lower in the liver and kidney mitochondria, leading to accumulation of glyoxylate in the tissues and its excretion in the urine. Part of the accumulated glyoxylate is converted to oxalate, causing hyperoxaluria.
 ...
PMID:Oxalate metabolism in thiamine-deficient rats. 342 52

Type I hyperoxaluria results from reduced activity of alpha-ketoglutarate: glyoxylate carboligase, which is necessary for the synergistic decarboxylation of glyoxylate and alpha-ketoglutarate to alpha-hydroxy-beta-keto-adipate. Since thiamine pyrophosphate is a cofactor in the reaction, thiamine deficiency might be expected to result in tissue oxalosis. However, there was no significant increase in the incidence of renal oxalosis in 15 patients with Wernicke's encephalopathy at necropsy compared with controls. It is possible that hyperoxaluria was present in these thiamine-deficient patients but at a urine concentration below that necessary for calcium oxalate deposition. It is also possible that the severity of the thiamine deficit required for hyperoxaluria exceeds that for the neuronal and cardiac manifestations.
 ...
PMID:Thiamine deficiency and oxalosis. 437 Dec 54