The effect of alanine infusions on growth hormone, insulin, and glucose in protein-calorie malnutrition.

In view of the previously reported inverse correlation between the elevated serum growth hormone (HGH) and low alanine in children with protein-calorie malnutrition (PCM), 30-min alanine infusions were performed in five children with PCM and 12-hr infusions in four children before and after therapy. These infusions did not lower basal HGH or improve its glucose suppressibility in untreated PCM, excluding a feedback relationship between HGH and alanine. There was no insulinotropic effect during 30-min infusions, but an improved insulin response to glucose after the 12-hr alanine infusion was found in three of four children before therapy. Plasma glucose rose slightly during alanine infusion in three of five children before treatment, but the magnitude of change was small and the relevance unclear.

Pancreatic islets of malnourished rats: quantitative histologic and electron microscopic findings.

Young rats were maintained for three weeks on a low-protein diet. These animals developed many of the features of human protein-calorie deficiency, including dextrose intolerance and diminished insulin release. Quantitative histologic and ultrastructural studies showed that malnourished rats had (1) a reduced total pancreatic islet volume, and (2) a preponderance of pale granules in the B cells. It is suggested that pale B granules may contain increased amounts of insulin, which accumulate in the cells because of defective insulin release. The mechanism responsible for this has not been elucidated.

Glucose tolerance and insulin release in malnourished rats.

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a 'functional immaturity' of the pancreas.

Early insulin release and its response to potassium supplementation in protein-calorie malnutrition.

Early insulin release after oral glucose is absent in protein-calorie malnutrition (PCM). There is an increase of the insulin-glucose ratio at 10 and 15 min induced by potassium supplementation compared to a similar group receiving an identical diet without supplementary potassium. This suggests that impaired insulin secretion in PMC is in part due to a potassium mediated disturbance of insulin release.