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I. Experiments in children and in animals seem to demonstrate that in marasmic malnutrition there is a reduction in the secretion of growth hormone. T o study this problem the fasting, resting plasma concentrations of growth hormone were determined, before, and 45 and 60 min after, stimulation with an intravenous dose of arginine, in six infants with marasmus, in six infants with kwashiorkor and in five normal infants. 2.The values of plasma growth hormone (4.1 k 0 . 9 7 ng/ml) in marasmic infants were significantly (P < o.001) lower than those of the controls (7.8 k 2.6 nglml), and responded little to stimulation with arginine (5.1 and 5.8 ng/ml at 45 and 60 min respectively), in contrast to those in the control group, which rose to 16.4 and 14.6 ng/ml. In children with kwashiorkor the values were very variable, but generally high, and showed little response (25.6 13.3 before and 25.0 f 17.6 and 14.2 f 5.3 ng/ml at 45 and 60 min after stimulation respectively).3. These results demonstrate that the responses of the hypophysis to deprivation of calories and protein (marasmus) and to protein deprivation (kwashiorkor) are different: in marasmus there is a progressive adaptation, with low secretion and poor reaction to stimulation, whereas in kwashiorkor the process is acute with high basal values of plasma growth hormone.

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Insulin-stimulated glucose uptake into muscle is depressed by high-fat-sucrose (HFS) feeding of rats. To investigate the mechanism of this insulin resistance, the in vivo activation of the insulin receptor kinase in liver and muscle of control and HFS-fed rats was determined. Rats were injected with glucose and insulin and killed 0, 5, 15, and 30 min after injection. Insulin binding was not changed in partially purified receptors from muscle of HFS rats. In control rats insulin receptor kinase activity was maximally stimulated threefold in liver at 5 min and fourfold in muscle at 15 min after insulin-glucose injection. The insulin-stimulated tyrosine kinase activity of receptors isolated from the liver of rats fed the HFS diet was decreased by 30% in comparison with the controls. In contrast, receptors isolated from muscle did not show any difference in basal or insulin-stimulated kinase activity between HFS-fed and control rats. Decreased in vivo activation of the insulin receptor kinase may be at least partially responsible for insulin resistance in liver. Because insulin binding and insulin stimulation of receptor kinase were normal in muscle of HFS-fed animals, it is concluded that the insulin resistance of glucose uptake into muscle is caused by a defect distal to the insulin receptor.

The histological aspect and the mitotic index of jejunal biopsies were studied in 8 normal infants, in 18 marasmic infants, and in 10 infants with kwashiorkor. The mucosa of the marasmic infants was similar to the normal controls, although thinner. In kwashiorkor the mucosa was similar to celiac disease. In marasmic infants fed on the same diet, the mitotic index is significantly lower in infants who do not show weight increase when compared with those who do increase in weight. In kwashiorkor the mitotic index is closer to, although also significatively lower than, normal. It is suggested that these differences are due to the low caloric intake in marasmus where the energy supply is not sufficient to maintain the rate of cell proliferation; a hormonal mechanism governed by the pituitary gland is also suggested. In kwashiorkor the histological aspect similar to celiac disease seems to indicate a common pattern of reaction of the jejunal mucosa due to different causes.