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ATP Depletion, a Possible Role in the Pathogenesis of Hyperuricemia in Glycogen Storage Disease Type I

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ATP Depletion, a Possible Role in the Pathogenesis of Hyperuricemia in Glycogen Storage Disease Type I ATP Depletion, a Possible Role in the Pathogenesis of Hyperuricemia in Glycogen Storage Disease Type I Harry L. Greene, … , Thomas H. Claus, Ian M. Burr J Clin Invest. 1978;62(2):321-328. https://doi.org/10.1172/JCI109132. Research Article Other investigators have shown that fructose infusion in normal man and rats acutely depletes hepatic ATP and Pi 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 glucose-6-phosphatase deficiency (GSD-I) as a result of ATP consumption during glycogenolysis and resulting excess glycolysis. The postulate was tested by measurement of: (a) hepatic content of ATP, glycogen, phosphorylated sugars, and phosphorylase activities before and after increasing glycolysis by glucagon infusion and (b) plasma urate levels and urate excretion before and after therapy designed to maintain blood glucose levels above 70 mg/dl and thus prevent excess glycogenolysis and glycolysis. Glucagon infusion in seven patients with GSD-I caused a decrease in hepatic ATP from 2.25 ± 0.09 to 0.73 ± 0.06 μmol/g liver (P <0.01), within 5 min, persisting in one patient to 20 min (1.3 μmol/g). Three patients with GSD other than GSD-I (controls), and 10 normal rats, showed no change in ATP levels after glucagon infusion. Glucagon caused an increase in hepatic phosphorylase activity from 163 ± 21 to 311 ± 17 μmol/min per g protein (P <0.01), and a decrease in glycogen content from 8.96 ± 0.51 to 6.68 ± 0.38% weight (P <0.01). Hepatic content of phosphorylated hexoses measured in […] Find the latest version: https://jci.me/109132/pdf ATP Depletion, a Possible Role in the Pathogenesis of Hyperuricemia in Glycogen Storage Disease Type I HARRY L. GREENE, FREDERICK A. WILSON, PATRICK HEFFERAN, ANNIE B. TERRY, JOSE ROBERTO MORAN, ALFRED E. SLONIM, THOMAS H. CLAUS, and IAN M. BURR, Departments of Pediatrics, Medicine, and Physiology, Vanderbilt Medical Center, Nashville, Tennessee 37232 A B S T R A C T Other investigators have shown that except for glucose-6-phosphate, returned toward pre- fructose infusion in normal man and rats acutely de- infusion levels within 20 min. pletes hepatic ATP and Pi and increases the rate of uric Treatment consisted of continuous intragastric feed- acid formation by the degradation of preformed nucleo- ings of a high glucose dietary mixture. Such treatment tides. We postulated that a similar mechanism of ATP increased blood glucose from a mean level of 62 (range depletion might be present in patients with glucose-6- 28-96) to 86 (range 71-143) mg/dl (P < 0.02), decreased phosphatase deficiency (GSD-I) as a result of ATP con- plasma glucagon from a mean of 190 (range 171-208) sumption during glycogenolysis and resulting excess to 56 (range 30-70) pg/ml (P < 0.01), but caused no sig- glycolysis. The postulate was tested by measurement nificant change in insulin levels. Urate output meas- of: (a) hepatic content of ATP, glycogen, phosphoryl- ured in three patients showed an initial increase, coin- ated sugars, and phosphorylase activities before and ciding with a decrease in plasma lactate and triglyceride after increasing glycolysis by glucagon infusion and levels, then decreased to normal within 3 days after (b) plasma urate levels and urate excretion before and treatment. Normalization of urate excretion was asso- after therapy designed to maintain blood glucose levels ciated with normalization of serum uric acid. above 70 mg/dl and thus prevent excess glycogenolysis We suggest that the maintenance of blood glucose and glycolysis. levels above 70 mg/dl is effective in reducing serum Glucagon infusion in seven patients with GSD-I urate levels and that transient and recurrent depletion caused a decrease in hepatic ATP from 2.25±0.09 to of hepatic ATP due to glycogenolysis is contributory 0.73±0.06 ,umol/g liver (P < 0.01), within 5 min, per- in the genesis of hyperuricemia in untreated patients sisting in one patient to 20 min (1.3 ,mol/g). Three pa- with GSD-I. tients with GSD other than GSD-I (controls), and 10 normal rats, showed no change in ATP levels after glu- INTRODUCTION cagon infusion. Glucagon caused an increase in hepatic phosphorylase activity from 163±21 to 311±17 ,umol/ The hyperuricemia associated with glycogen storage min per g protein (P < 0.01), and a decrease in glycogen disease type I (GSD-I)' or glucose-6-phosphatase de- content from 8.96±0.51 to 6.68±0.38% weight (P < 0.01). ficiency, is often of such severity that it produces gout Hepatic content of phosphorylated hexoses measured and its ensuing complications (1, 2). Although several in two patients, showed the following mean increases investigators have demonstrated an excess production in response to glucagon; glucose-6-phosphate (from of uric acid from increased synthesis of purines de novo 0.25 to 0.98 ,umol/g liver), fructose-6-phosphate (from (2-7), the precise mechanism giving rise to this anom- 0.17 to 0.45,umol/g liver), and fructose-1,6-diphosphate aly has not been elucidated. (from 0.09 to 1.28 within 5 min. These changes, Roe and Kogut (6) recently showed that within 30 min tmol/g) after an injection of glucagon, patients with GSD-I were unique in showing a significant increase in plasma Dr. Burr and Dr. Wilson are investigators for the Howard uric acid levels and a two to threefold increase in excre- Hughes Medical Institute. Dr. Terry's present address is the tion of urate. This observation suggested that such a Department of Pediatrics, University of Oregon Health in Science Center, Portland, Oreg. 97201. Dr. Hefferan's present rapid increase urate levels resulted primarily from address is the Department of Pediatrics, University of Texas, enhanced nucleotide catabolism rather than from a Houston, Tex. Received for publication 15 July 1977 and in revised form IAbbreviations used in this paper: G-6-P, glucose-6-phos- 3 April 1978. phate; GSD-I, glycogen storage disease type I. J. Clin. Invest. © The American Society for Clinical Investigation, Inc., 0021-9738/78/0801-321 $1.00 321 direct effect on the rate of purine synthesis as originally of hypoglycemia, we have used glucagon administra- suggested by Howell (7). Thus, the observed increase tion to simulate some of the biochemical changes re- in de novo synthesis of purines in GSD-I would ap- sulting from hypoglycemia: e.g., activation of phos- pear to be secondary to the increased rate of purine phorylase, and reduction in hepatic glycogen. In addi- catabolism. Such a sequence has been shown to occIur tion to the glucagon-induced changes, glucose therapy after fructose infusions in normal man (8-10) and rats given in quantities to prevent frequent and recurrent (11-13). Although the metabolic sequences are com- episodes of low blood glucose concentrations, should plex, a series of publications has shown that phosphoryl- decrease the elevated seruim uric acid levels (16). This ation of large amounts of fructose leads to acute de- report presents the results of glucagon-indtuced changes pletion of hepatic ATP and Pi levels, which in turn in glycogen content, phosphorylase activity, and ATP favor degradation of preformed AMP to uric acid (8-13). concentration in seven patients with GSD-I, two of The similarity between the blood chemistries of pa- which also had measiurements of G-6-P, fiuctose-6- tients with GSD-I and subjects infused with fructose phosphate, and fructose-1, 6-diphosphate. In addition, (hypertriglyceridemia lacticacidemia, hypophospha- the effect of continuouis glucose therapy on uric acid temia, and hyperuricemia), prompted the hypothesis excretion and plasma uirate levels was meassured. The that the mechanism for hyperuricemia in these two findings provide stupport for the hypothesis that in- conditions might be analogous (6, 14). For example, creased degradation of preformed purines is important patients with GSD-I can degrade glycogen to glucose- in the genesis of hyperuiricemia in GCSD-I. 6-phosphate (G-6-P) but because of the enzyme defect, hydrolysis to glucose and Pi is impaired. Frequent peri- METHODS ods of hypoglycemia should therefore stimulate the for- Patient .studies. The patient group consisted of 10 pa- mation of large amounts of G-6-P which escapes pri- tients (ages 18 mo to 19 yr) with hepatic glycogen accumula- marily through the Embden-Meyerhof pathway to be tion. Seven patients had the clinical and laboratory features further phosphorylated utilizing equimolar amounts of of GS D-I and deficient glucose-6-phosphatase activity (group I). ATP (15) (see Fig. 1). Thus, both fructose infusion in Of the remaining three patients, one had debrancher enzyme normal man and (amylo-1-4,1-6-glucosidase) deficiency (type III-GSD) and the hypoglycemia in patients with GSD-I other two had excessive hepatic glycogen content without a should result in an increase in phosphorylated stugars detectable defect in glycogenolytic enzyme activities (group and a decrease in ATP and Pi in the liver. II). These latter patients showed the expected glycemic re- Demonstration that patients with GSD-I have low sponse to glucagon. All patients were admitted to the Clinical hepatic levels of ATP and and high levels of phos- Research Center of Vanderbilt University Hospital for de- Pi finitive diagnosis and treatment of GSD. They were main- phorylated sugars, during periods of hypoglycemia, tained on a diet consisting of 60% starch or glucose and <50 would support this postulate. Since it is not medically mg purine/100 g of food daily (17). Daily calorie-protein in- feasible to obtain hepatic tisssue samples during periods take varied letween patients because of age differences; the range was between 45 and 65 kcal/kg body wt.
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