hyperuricemia/phosphatase

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A hypothesis linking hypoglycemia, hyperuricemia, lactic acidemia, and reduced gluconeogenesis in alcoholics to inactivation of glucose-6-phosphatase activity by acetaldehyde.

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Preliminary data have been obtained indicating that glucose-6-phosphatase is inactivated upon preincubation with 447 and 224 mM acetaldehyde for 30 min at room temperature, resulting in a loss of 67% and 33% of the original activity, respectively. The reaction with acetaldehyde is rapid because 44%

Hyperuricemia in glycogen storage disease type I. Contributions by hypoglycemia and hyperglucagonemia to increased urate production.

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Studies were performed to determine whether hypoglycemia or the glucagon response to hypoglycemia increases uric acid production in glycogen storage disease type I (glucose-6-phosphatase deficiency). Three adults with this disease had hyperuricemia (serum urate, 11.3-12.4 mg/dl) and reduced renal

The serum apolipoprotein profile of patients with glucose-6-phosphatase deficiency.

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Abnormal lipid transport is one of the more severe pathophysiological manifestations of glucose-6-phosphatase deficiency (glycogen storage disease, type I: GSD-I). To characterize further lipoprotein abnormalities in this inborn error of glycogen metabolism, we determined the levels of serum

Combined deficiency of glucose-6-phosphatase and fructose-1, 6-diphosphatase. Studies of glucagon secretion and fuel utilization.

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An adult woman with hypoglycemia, hyperlactatemia, hyperuricemia, hypertriglyceridemia, hyperketonemia and inability to make new glucose from galactose, fructose, glycerol and alanine was found to have no hepatic glucose-6-phosphatase and deficient fructose-1,6-diphosphatase. Nonautonomous

ATP depletion, a possible role in the pathogenesis of hyperuricemia in glycogen storage disease type I.

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Other investigators have shown that fructose infusion in normal man and rats acutely depletes hepatic ATP and P(i) and increases the rate of uric acid formation by the degradation of preformed nucleotides. We postulated that a similar mechanism of ATP depletion might be present in patients with

Variation of rat serum biochemical values following decapitation or anesthesia with ether, halothane or Innovar-VetR: rapid Innovar-VetR-induced hyperuricemia and hyperglycemia.

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True reference values (TRV) should ultimately be determined in blood from inactive, unstimulated rats but in practice, acceptable reference values (ARV) may be established using blood from decapitated or anesthetized animals if one is cognizant of variations associated with blood sampling

Sustained hepatic and renal glucose-6-phosphatase expression corrects glycogen storage disease type Ia in mice.

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Deficiency of glucose-6-phosphatase (G6Pase), a key enzyme in glucose homeostasis, causes glycogen storage disease type Ia (GSD-Ia), an autosomal recessive disorder characterized by growth retardation, hypoglycemia, hepatomegaly, nephromegaly, hyperlipidemia, hyperuricemia, and lactic acidemia.

Heterogeneous mutations in the glucose-6-phosphatase gene in Japanese patients with glycogen storage disease type Ia.

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Glycogen storage disease type Ia (GSD-Ia) is an autosomal recessive disorder of glycogen metabolism caused by glucose-6-phosphatase (G6Pase) deficiency. It is characterized by short stature, hepatomegaly, hypoglycemia, hyperuricemia, and lactic acidemia. Various mutations have been reported in the

Relationship between serum uric Acid and bone mineral density in the general population and in rats with experimental hyperuricemia.

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Higher serum uric acid concentrations have been associated with higher bone mineral density (BMD) in observational studies of older men and perimenopausal or postmenopausal women, prompting speculation of a potential protective effect of uric acid on bone. Whether this relationship is present in the

Hyperuricemia has an adverse impact on the prognosis of patients with osteosarcoma.

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Patients with osteosarcoma have poor prognosis and are often at high risk of death. Identification of prognostic biomarkers for osteosarcoma may aid in improving the survival. Hyperuricemia had been suggested as a poor prognostic factor of several cancers, but the prognostic role of hyperuricemia in

Effects of acupuncture at Shu, Yuan, and Mu acupoints on blood serum uric acid and xanthine oxidase levels in a rat model of gout and hyperuricemia.

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To investigate the effects of needling the Shu, Yuan, and Mu acupoints on serum uric acid (SUA), xanthine oxidase (XOD), and alkaline phosphatase (ALP) levels and the kidney index in a rat model of gout and hyperuricemia.Fifty rats were randomly divided

[Definition and classification of hyperuricemia].

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Hyperuricemia (serum urate level >7 mg/dL) is caused by accelerated generation of uric acid and/or impaired excretion in the kidney. It is classified into three types (overproduction, underexcretion and mixed types). The typical cases with the type of uric acid overproduction are hypoxanthine

Type I glycogen storage diseases: disorders of the glucose-6-phosphatase complex.

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Glycogen storage disease type I (GSD-I) is a group of autosomal recessive disorders with an incidence of 1 in 100,000. The two major subtypes are GSD-Ia (MIM232200), caused by a deficiency of glucose-6-phosphatase (G6Pase), and GSD-Ib (MIM232220), caused by a deficiency in the glucose-6-phosphate

Mutations in the glucose-6-phosphatase-alpha (G6PC) gene that cause type Ia glycogen storage disease.

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Glucose-6-phosphatase-alpha (G6PC) is a key enzyme in glucose homeostasis that catalyzes the hydrolysis of glucose-6-phosphate to glucose and phosphate in the terminal step of gluconeogenesis and glycogenolysis. Mutations in the G6PC gene, located on chromosome 17q21, result in glycogen storage

The independent association between parathyroid hormone levels and hyperuricemia: a national population study.

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BACKGROUND Increased frequencies of hyperuricemia and gout have been associated with primary hyperparathyroidism, and recent clinical trials of parathyroid hormone (PTH) have reported hyperuricemic adverse events. We evaluated the potential population impact of PTH on serum uric acid (SUA) levels by

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