The effect of DPT inoculation on the hormonal control of glucose homeostasis in children recovered from malnutrition

The effect of a controlled stress (DPT inoculation) on the hormonal control of glucose homeostasis was investigated in children nutritionally rehabilitated from severe malnutrition. The age range of the 15 children studied was 6-26 months. Plasma insulin (INS), growth hormone (GH) and interleukin-1 (IL-1) were measured by radioimmunoassay; plasma glucose (GLU) by a glucoseoxidase method; and red cell insulin binding ( percentSB) was determined, using A-14 monoiodinated insulin. Measurements were made on two occasions: (T-O) at 10 a.m.,12 hr before DPT inoculation, and (T-36) 36 hr. after inoculation. On both occasions, 4 hr post-prandial blood samples were used, and the mean body temperature(T) on the day of the test was determined. Red cell insulin binding ( percentSB) was significantly higher at T-36 than at T-O (16.8 ñ 1.7 vs 12.1 ñ 1.2 (14), p=0.005). (Results were expressed as mean ñ SEM, numbers of paired observations in parentheses). The higher percentSB after DPT was accompanied by an increase in the number of receptor sites (S) (29.05 ñ 6.5 vs 15.6 ñ 2.5 (14),p=0.025). However, insulin receptor affinity (K x 10(9)M(-1)) was decreased 0.7 ñ 0.1 vs 1.5 ñ 0.3(14), p=0.008). There were no significant differences in the plasma levels of insulin, glucose and interleukin-1, but plasma growth hormone (æU/ml) was increased after DPT, (18.0 ñ 3.0 vs 11.5 ñ 1.2 (13), p=0.04). Body temperature (§C) was also significantly increased after DPT,(99.9 ñ 0.4 vs 98.3 ñ 0.2(14), p=0.006). The change in plasma glucose from T-O to T-36 tended to be associated with both a change in plasma insulin (p=0.06) and plasma growth hormone (p=0.07). Increased insulin binding, as one index of increased insulin sensitivity during fever, can contribute to a reduction in blood glucose. However, the elevation in plasma growth hormone cold buffer the hypoglycaemic effect of insulin, and help to maintain glucose homeostasis (AU)

Fasting pancreatic glucagon in Jamaican children during malnutrition and subsequent recovery

Fasting pancreatic glucagon was observed in Jamaican infants during malnutrition and subsequent recovery. Rehabilitation in two groups of children with isocaloric diets rich either in carbohydrate or fat produced no differences in the rate of weight gain. During malnutrition, plasma pancreatic glucagon concentration was 104ñ11 (n=20) pg/ml (meanñS.E.) significantly lower than during recovery when the maximum value was 180ñ24 (n=13) pg/ml during the later recovery phase. After clinical recovery glucagon levels declined to 127ñ13 (n=15) pg/ml. Plasma insulin followed a similar pattern, increasing significantly during catch-up growth and declining after recovery. Slower rates of growth were associated with the simultaneous decline in the concentrations of both hormones after clinical recovery. (Summary)

A comparison of fasting plasma insulin and growth hormone concentrations in marasmic, kwashiorkor, marasmic-kwashiorkor and underweight children

Fasting plasma insulin and growth hormone concentrations were measured in 24 marasmic, 11 kwashiorkor, 16 marasmic-kwashiorkor, and 4 underweight children. Hormone measurements were made by a special modification of the Hales and Randle double antibody immunoassay with increased sensitivity in the concentration range 0-25 æU/ml. Fasting plasma insulin was low in marasmus, kwashiorkor, and marasmic-kwashiorkor children, and increased to normal levels after recovery. Fasting plasma growth hormone was elevated in all groups during nutrition and was significantly decreased to normal levels after recovery. There were no significant differences in plasma insulin or growth hormone levels between the different clinical types of severe protein malnutrition. These hormonal changes in severe protein energy malnutrition are of complex and not fully understood etiology. However, recovered children appear to have a hormonal pattern similar to that described in normal control infants and children. (Summary)

Insulin, growth hormone and carbohydrate tolerance in Jamaican children rehabilitated from severe malnutrition

Intravenous glucose tolerance tests were carried out in 20 children (aged 6 - 24 mo) clinically recovered from severe malnutrition. Blood samples were obtained between 10 am and 11 am after 16 hr fast, from a peripheral vein kept patent by a slow infusion of 0.9 percent saline. Samples were taken at timed intervals: 0, 1, 2, 3, 5, 7, 10, 20, 30, 40 and 50 min after IV injection of glucose (0.5 g/kg body weight). Plasma insulin, growth hormone, and glucose were measured. Total responses were expressed as the sum of the values at each time point. The mean rate of glucose removal (KG percent/min) was 2.28 +/- 0.13. This is within the normal published range of 2 to 3.5. Four children were < 1 SD below the mean. In these four children, fasting growth hormone and total growth hormone response were significantly higher (p>0.001) than in the others. There was a wide range for fasting growth hormone: 1-91 uU/ml. There was a negative correlation between KG and total growth hormone response (r = -0.64, p<0.05, n = 12), and between KG and age (r = -0.61, p<0.01, n = 20). In three children fasting glucose was abnormally low. Neither fasting insulin (3.04 +/- 0.33 uU/ml), fasting glucose (3.9 +/- 0.16 mmol/L) nor insulin response were significantly related to KG. Peak insulin was 28.2 +/_ 2.7 uU/ml and peak glucose was 18.5 +/- 0.6 mmol/L. Seven children showed a delayed (5-10 min) insulin response to glucose: 13 had a prompt insulin response 1 min after glucose. The KG of those children who had a delayed insulin response to glucose was normal, but the KG of 2 children with an abnormally low insulin response was below normal. Thus, after anthropometric recovery from malnutrition, 20 percent of children had a low KG, associated with an elevated growth hormone response. In 30 percent of children the insulin response to glucose was delayed, but this was not related to the glucose disappearance rate. In 10 percent of the children, the insulin response to glucose was abnormally low, and this was associated with low KG. In 15 percent of the children, fasting glucose concentrations were abnormally low. Abnormal carbohydrate tolerance was associated with low insulin output and/or elevated growth hormone concentration. (Summary)