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)

Role of intracellular sodium in the hypertension of pre-eclampsia - abstract

Patients with pre-eclampsia have abnormal sodium homeostasis. This is so at the level of the whole body as well as at a cellular level. We have described in such patients raised leucocyte sodium content and lowered potassium which are probably related to slowing of the sodium pump (Forrester and Alleyne, 1980, Clinical Science 59: 199-201). In order to investigate whether the abnormal cell sodium content was causally related to blood pressure elevation, we prospectively measured leucocyte sodium content and blood pressure in 85 obstetrically normal primigravidae. Seven developed pre-eclampsia. In these patients both blood pressure and cell sodium rose pari passu up to delivery and fell post partum. A similar but smaller trend was seen in controls. Thus pre-eclampsia was associated with exaggerated changes in cell sodium content which paralleled blood pressure changes. Cell potassium content fell in both groups but to a greater extent in pre-eclamptics. (Seon and Forrester, 1988, Clinical Science 75: in press). Patients who developed pre-eclampsia had higher blood pressure and cell sodium at six weeks post partum, suggesting that the pregnancy changes had not fully resolved. We therefore cross-sectionally measured blood pressure and leucocyte sodium content in patients who had had pre-eclampsia and delivered 40 weeks previously and compared them with matched controls (Forrester et al, Clinical Science, in press). Raised intracellular sodium can cause high blood pressure by raising peripheral resistance. We propose that this is a probable mechanism for blood pressure changes in pre-eclampsia (AU)

Zinc absorption in malnutrition - abstract

Malnourished children are often zinc-deficient. Net intestinal absorption (NA) of zinc is the main factor controlling zinc status: NA = TA - ES, where TA is total intestinal absorption, and ES is endogenous secretion of zinc into the intestine. In order to investigate factors affecting zinc homeostasis, we have measured NA and TA in 7 severely malnourished and in 10 recovered (weight-for-height) children, 8 to 18-months-old. NA was calculated as the difference between feed zinc intake and faecal zinc output over a 3-day period. TA was calculated as the difference between feed intake and faecal output of the stable isotope, 70Zn, given over the first 6 hours of the balance. Eight of the recovered children, the control group, were given a standard cow's milk-based infant formula at 'maintenance energy' intake. TA of zinc was 25ñ7 percent of zinc intake (meanñSD); it increased significantly with the age and weight of the child, and insignificantly with the weight gain (RWG). NA of zinc, 19ñ8 percent of zinc intake, was not related to age, weight or RWG. ES of zinc varied from 0 to 22 percent of zinc intake. The other 2 recovered children were given a low protein formula, also at 'maintenance energy' intake. Of them, 4 non-oedematous children had RWG similar to the recovered children but NA of zinc (8ñ4 percent of intake) was lower than in the recovered children. TA (32ñ1 percent of intake) was lower than in the 2 recovered children on the same formula. The 3 oedematous children were sicker than the others; two were anorectic and therefore fed by nasogastric tube throughout their balances. TA were 5 and 9 percent in the tube fed and 21 percent in the other child. NA of zinc was -28, +2 and -14 percent. Thus 2 children had a high ES of zinc while the other child had a low ES Zn; he was the only one with profuse diarrhoea. The very low TA Zn and negative NA in two of the three children show that zinc homeostasis was markedly deranged and that zinc deficiency was probably present. This is consistent with our previous finding of low plasma zincs in oedematous malnourished children. The findings imply the need for zinc supplementation of severely malnourished children, in particular those with oedema. They also imply that factors affecting zinc absorption include the child's age and/or weight, and the dietary zinc and/or protein content. This study was supported by the Medical Research Council and the Wellcome Trust (AU)

Red cell sodium metabolism in human hypertension - abstract

A derangement in cell sodium homeostasis has been reputed to be the cause of primary hypertension in man. This hypothesis is supported by findings of raised intracellular sodium and suppressed sodium pump activity. These findings, however, are not universal. These experiments were designed to measure red cell sodium and potassium content and sodium transport activity as well as to define the role of plasma in these transport activities. Twelve hypertensives and 27 normotensive controls were subjected to venipuncture. Red cells were separated from plasma and the cellular content of sodium and potassium was measured. Na efflux from loaded cells was used to measure sodium pump activity and contransport. Red cell sodium content was slightly higher in hypertensive patients (10.4ñ2.8 vs 8.7ñ2.1 mMOl/l RBC, p<.05). Red cell potassium was the same in both groups (110ñ7 vs 113ñ8 mMOl/l RBC). Ouabain-sensitive sodium efflux, a measure of sodium pump activity, was the same in hypertensives and normotensives (6.69ñ2.57 vs 6.57ñ2.34 mMol/l /RBC/h). Plasma incubation produced an across-the-board reduction in sodium transport activities. Ouabain-sensitive efflux was 5.79ñ3.05 vs 4.23ñ2.66, and contransport, 0.57ñ0.28 vs 0.63ñ0.27 mMol/l RBC/h in hypertensives and normotensives respectively. We conclude that red cell sodium homeostasis is virtually identical in hypertensives and normotensives and that a circulating inhibitor is present to the same degree in both their plasmas. These data do not support the hypothesis that essential hypertension is causally associated with derangements of cell sodium metabolism (AU)

Electrolyte metabolism in the colon - abstract

Studies were designed to determine the role of the colon in electrolyte homeostasis, and to analyse some of the factors which affect electrolyte transport in the colon. These studies were carrried out in humans by the analysis of faecal fluid electrolytes, and in rats and dogs by in-vivo isolated loops of colon. The results obtained show that, particularly under conditions of electrolyte depletion, the colon plays an important role in electrolyte homeostasis. There is a suggestion that although there is a relationship between the transport of sodium and potassium, transport of potassium may occur independently of sodium transport. There may be a relationship between the transport of potassium and bicarbonate and there is a relationship between the transport of chloride and bicarbonate (AU)