Reversible changes of the muscle cell in experimental phosphorus deficiency.

Fuller, Thomas W.; Carter, N W; Barcenas, Camilo G.; Knöchel, James P.

doi:10.1172/jci108343

Cited by 127 publications

(47 citation statements)

References 20 publications

(23 reference statements)

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“…For this purpose, the mitochondrial isolation procedure was moodified by addition of 1 (33); the chicks were fe(r a (liet containing slightly mnore phosphorus tha.n starter mlash, were not hvpophiosphateinic, ancd mulsele phosphate (Table II) was not significaiitly differenit froml that of 3-wk vitamin)il -treated chicks or starter-mash cointrols. Although in previous studies vitaminii 1)-deficient rats were foundl to have lower skeletal musele ATP concentrations than vitaimin D-treatedI coontrols (24,25), coomparisoni of ATP contents of group 1-noD ann group 4-1) 2 wk chick skeletal miuscles by the freeze-clamilp techni(que (11) showe(d no significaiit differenices in our study.…”

Section: Resultsmentioning

confidence: 99%

Skeletal Muscle Calcium Metabolism and Contractile Force in Vitamin D-deficient Chicks

Pleasure¹,

Wyszynski²,

Sumner³

et al. 1979

J. Clin. Invest.

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Section: Resultsmentioning

confidence: 99%

Skeletal Muscle Calcium Metabolism and Contractile Force in Vitamin D-deficient Chicks

Pleasure¹,

Wyszynski²,

Sumner³

et al. 1979

J. Clin. Invest.

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“…Earlier reports have suggested that rhabdomyolysis may be related to a state of cellular phosphate depletion [19][20][21]. During insulin treatment of diabetic ketoacidosis, a precipitous fall in serum phosphate often occurs due to the transfer of phosphate from the extracellular to the intracellular compartment [22].…”

Section: Discussionmentioning

confidence: 99%

Nontraumatic rhabdomyolysis during diabetic ketoacidosis

Møller-Petersen

Pt²,

Hjörne

et al. 1986

Diabetologia

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Summary. The frequency of nontraumatic rhabdomyolysis in diabetic ketoacidosis was investigated by serial measurements of the serum levels of myoglobin and the serum activity of creatine kinase isoenzyme MM in 12 consecutively admitted ketoacidotic patients. In 5 patients (Group 1) we found hypermyoglobinaemia and elevated activity of creatine kinase isoenzyme MM on admission to hospital, whereas these two variables were normal in 7 patients (Group 2). On admission significantly higher median blood glucose levels and higher median serum osmolality were found in Group 1 than in Group 2 (for blood glucose: 49.6 mmol/1 versus 19.0 mmol/1, p<0.02; for serum osmolality: 360mosm/kg H20 versus 315 mosm/kg H20, p <0.05). Decreased renal function was found in Group 1 as reflected by significantly higher betarmicroglobulin serum concentrations in Group 1 compared with Group 2 on admission (median values 4.1 mg/1 versus 1.7 mg/1, p < 0.01) and during the first 3 days of therapy. The serum concentration of hypoxanthine (an indicator of the cellular energy state) was elevated in all patients on admission, with no difference between patients with or without hypermyoglobinaemia. In conclusion, our findings suggest that nontraumatic rhabdomyolysis with hypermyoglobinaemia and elevated serum activity of creatine kinase isoenzyme MM may be a hitherto unrecognized common feature of diabetic ketoacidosis.

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“…Models that produce the greatest reductions in serum phosphorous concentration are associated with a more severe myopathy, which is characterized by muscle wasting, weakness with even modest activity, and diminished ATP levels in resting cardiac and skeletal muscle (10,11,13,16,17,22). Even in these severely phosphate-deficient animals, the myopathy is reversible following phosphate supplementation (10,16).…”

Section: Discussionmentioning

confidence: 99%

“…These studies suggest that INTRODUCTION Hypophosphatemia and intracellular deficiency of inorganic phosphate result in dysfunction of a wide range of organ systems in man and experimental animals. Erythrocyte hemolysis (1-3), derangements in the mechanical and phagocytic properties of leukocytes (1, 4), decreased survival and abnormal function of platelets (1,5), central nervous system abnormalities compatible with metabolic encephalopathy (1,6,7), abnormalities in renal function (1,8), and cardiac (1,(9)(10)(11)13), and skeletal myopathy (1,(12)(13)(14)(15)(16)(17) have been described in patients or animals with phosphate deficiency.…”

mentioning

confidence: 99%

Defective adenosine triphosphate synthesis. An explanation for skeletal muscle dysfunction in phosphate-deficient mice.

Hettleman¹,

Sabina²,

Drezner³

et al. 1983

J. Clin. Invest.

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A B S T R A C T The basis for skeletal muscle dysfunction in phosphate-deficient patients and animals is not known, but it is hypothesized that intracellular phosphate deficiency leads to a defect in ATP synthesis. To test this hypothesis, changes in muscle function and nucleotide metabolism were studied in an animal model of hypophosphatemia. Mice were made hypophosphatemic through restriction of dietary phosphate intake. Gastrocnemius function was assessed in situ by recording isometric tension developed after stimulation of the nerve innervating this muscle. Changes in purine nucleotide, nucleoside, and base content of the muscle were quantitated at several time points during stimulation and recovery.Serum concentration and skeletal muscle content of phosphorous are reduced by 55 and 45%, respectively, in the dietary restricted animals. The gastrocnemius muscle of the phosphate-deficient mice fatigues more rapidly compared with control mice. ATP and creatine phosphate content fall to a comparable extent during fatigue in the muscle from both groups of animals; AMP, inosine, and hypoxanthine (indices of ATP catabolism) appear in higher concentration in the muscle of phosphate-deficient animals. Since total ATP use in contracting muscle is closely linked to total developed tension, we conclude that the comparable drop in ATP content in association with a more rapid loss of tension is best explained by a slower rate of ATP synthesis in the muscle of phosphate-deficient animals. During the period of recovery after muscle stimulation, ATP use for contraction is minimal, since the muscle is at rest. In the recovery period, ATP content returns to resting levels more slowly in the phosphate-deficient than in the control animals. In association with the slower rate of ATP repletion, the precursors inosine monophosphate and AMP remain elevated for a longer period of time in the muscle of phosphate-deficient animals. The slower rate of ATP repletion correlates with delayed return of normal muscle contractility in the phosphate-deficient mice. These studies suggest that the slower rate of repletion of the ATP pool may be the consequence of a slower rate of ATP synthesis and this is in part responsible for the delayed recovery of normal muscle contractility.

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Reversible changes of the muscle cell in experimental phosphorus deficiency.

Cited by 127 publications

References 20 publications

Skeletal Muscle Calcium Metabolism and Contractile Force in Vitamin D-deficient Chicks

Skeletal Muscle Calcium Metabolism and Contractile Force in Vitamin D-deficient Chicks

Nontraumatic rhabdomyolysis during diabetic ketoacidosis

Defective adenosine triphosphate synthesis. An explanation for skeletal muscle dysfunction in phosphate-deficient mice.

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