We have studied changes in the IGF axis in an ovine model of myocardial infarction (MI), in order to determine the relationship between time-based changes in postinfarct myocardium and IGF levels. IGF localization was studied by immunocytochemistry, production by in situ hybridization, and specific binding by radioligand studies.

SUMMARY Leucine and alanine production rate was measured in 5 patients with acid maltase deficiency in the postabsorptive state, following 6 months on a normal diet with placebo and 6 months on an isocaloric high protein diet (16-22% protein). Whole body leucine production rate, a measure of protein degradation, expressed in terms of lean body mass was significantly greater than in five control subjects. Following the high protein diet, leucine production rate was decreased in four of the five patients but this was not statistically significant. Alanine production rate expressed in terms of lean body mass was significantly greater than in control subjects. After the high protein diet, alanine production rate and concentration were significantly decreased (p < 0O05). There were no significant improvements in any ofthe clinically relevant variables measured in these patients. It is possible that a larger increase in protein intake over a longer time period may have a clinical effect.Type II glycogenosis (acid alpha-1,4-glucosidase deficiency) presents either in infancy, or in juvenile or adult forms.' Infants are floppy and develop gross cardiomegaly and hepatomegaly before perishing in the first few years of life.2 Adults tend to present in their late 'teens or twenties with marked truncal and pelvic girdle weakness and impressive paraspinal muscle wasting. However, the key clinical feature is the presence of respiratory insufficiency which is chiefly caused by diaphragmatic weakness or paralysis.34 The diagnosis can be confirmed by finding absent or low levels of acid maltase in muscle,5 cultured skin fibroblasts6 and leucocytes.78The muscle wasting and weakness in the adult-onset disease has been attributed to the disruption of muscle fibres caused by accumulation of glycogen in the sarcoplasm.9 Measurement of protein turnover in a patient with this disorder has demonstrated an increase in whole body protein degradation which suggests that the myopathy may be due to increased muscle breakdown.'" Treatment of the patient with a

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