glycogen storage disease type vii/carbohydrate

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Abnormal oxidative metabolism and O2 transport in muscle phosphofructokinase deficiency.

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Humans who lack availability of carbohydrate fuels may provide important models for the study of physiological control mechanisms. We compared seven patients who had unavailability of muscle glycogen and blood glucose as oxidative fuels due to muscle phosphofructokinase deficiency (PFKD) with five

Glucose-induced exertional fatigue in muscle phosphofructokinase deficiency.

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BACKGROUND The exercise capacity of patients with muscle phosphofructokinase deficiency is low and fluctuates from day to day. The basis of this variable exercise tolerance is unknown, but our patients with this disorder report that fatigue of active muscles is more rapid after a high-carbohydrate

The potential of a ketogenic diet to minimize effects of the metabolic fault in glycogen storage disease V and VII

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Purpose of review: To explore the potential of a low carbohydrate ketogenic diet (LCKD) to counter physical activity intolerance, pain and muscle damage for glycogen storage disease (GSD) V and VII, and highlight the realistic possibility

[Metabolic myopathies].

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OBJECTIVE To review the metabolic myopathies manifested only by crisis of myalgias, cramps and rigidity of the muscles with decreased voluntary contractions and normal inter crisis neurologic examination in children and adolescents. METHODS These metabolic myopathies are autosomic recessive

Myogenic hyperuricemia: what can we learn from metabolic myopathies?

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The association of muscle glycogenosis with hyperuricemia led to the identification of a unique purine disorder. Myogenic hyperuricemia is ascribed to excessive degradation of muscle purine nucleotides, secondary to impaired ATP generation. Although this pathophysiological condition has been

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