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hyperuricemia/proline
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Association of plasma free amino acids with hyperuricemia in relation to diabetes mellitus, dyslipidemia, hypertension and metabolic syndrome.
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Previous studies demonstrated independent contributions of plasma free amino acids (PFAAs) and high uric acid (UA) concentrations to increased risks of lifestyle-related diseases (LSRDs), but the important associations between these factors and LSRDs remain unknown. We quantified PFAAs and UA
Effect of a traditional Chinese medicine prescription Quzhuotongbi decoction on hyperuricemia model rats studied by using serum metabolomics based on gas chromatography-mass spectrometry.
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Morbidity of hyperuricemia has constantly increased in population in decades, and hyperuricemia has proved to be an important risk factor for gout, cardiovascular diseases and others. Many urate-lowering drugs have unfavorable side effects and drug interactions. Quzhuotongbi decoction (QZTBD) is an
Metabolomic profiles delineate the effect of Sanmiao wan on hyperuricemia in rats.
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A serum metabolomic method based on ultra-high-performance liquid chromatography coupled with mass spectrometry was developed to characterize hyperuricemia-related metabolic profiles and delineate the mechanism of Sanmiao wan (SMW), a traditional Chinese medicine (TCM), in treating hyperuricemic
Nocturnal intragastric therapy in type I glycogen storage disease: effect on hormonal and amino acid metabolism.
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The acute hormonal and amino acid responses to differing food substrates were examined in type 1 glycogen storage disease. Ingestion of a glucose load or a glucose-plus-beef meal caused an acute fall in the initially elevated plasma glucagon, alanine, proline, and lactate. Ingestion of beef alone
HPRTSardinia: a new point mutation causing HPRT deficiency without Lesch-Nyhan disease.
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Hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency always causing hyperuricemia presents various degrees of neurological manifestations, the most severe which is Lesch-Nyhan syndrome. The HPRT gene is situated in the region Xq26-q27.2 and consists of 9 exons. At least 300 different
Stabilization of the predominant disease-causing aldolase variant (A149P) with zwitterionic osmolytes.
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Hereditary fructose intolerance (HFI) is a disease of carbohydrate metabolism that can result in hyperuricemia, hypoglycemia, liver and kidney failure, coma, and death. Currently, the only treatment for HFI is a strict fructose-free diet. HFI arises from aldolase B deficiency, and the most
Associations among amino acid, lipid, and glucose metabolic profiles in childhood obesity.
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