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Significant hormonal changes have been reported in childhood malnutrition, including high serum levels of growth hormone and cortisol, and low levels of circulating insulin. The ultrastructure of the endocrine pancreas in such patients has hitherto not been reported. A light microscopy survey of the pancreatic islets was carried out on 69 malnourished children dying from protein-energy malnutrition. In seven of these cases, a rapid autopsy protocol allowed tissues to be fixed for electron microscopy within 75 minutes of death. This paper presents the first ultrastructural observations on the Islets of Langerhans in childhood protein-energy malnutrition. In all cases, there was a variable degree of degeneration of all cell types with membrane damage, loss of ribosomes, vesiculation and mitochondrial swelling. In addition, the B-cells showed a high proportion of precursor granules compared to crystal forms, possibly accounting for low insulin serum levels reported by other workers. It is suggested that islet cell changes may be related to free radical damage secondary to depletion of glutathione and other antioxidants, as well as relative deficiencies of cysteine and zinc. In addition, the effects of agonal anoxia, and a short fixation delay after death must be considered.

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Insulin binding to erythrocyte receptors was compared in malnourished and control rats. Percentage specific insulin binding to malnourished rat erythrocytes was significantly lower than to control erythrocytes (P less than 0.001). The low insulin binding in the malnourished rat erythrocytes was accompanied by low insulin receptor affinity (P = 0.035).

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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 glucose oxidase method; and red cell insulin binding (%SB) was determined, using A-14 monoiodinated insulin. Measurements were made on two occasions: (T-0) 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 (%SB) was significantly higher at T-36 than at T-0 (16.8 +/- 1.7 vs 12.1 +/- 1.2 (14), p = 0.005). (Results were expressed as mean +/- SEM, numbers of paired observations in parentheses). The higher %SB after DPT was accompanied by an increase in the number of receptor sites (S) (29.05 +/- 6.5 vs 15.6 +/- 2.5 (14), p = 0.025). However, insulin receptor affinity (K x 10(9) M-1) was decreased (0.7 +/- 0.1 vs 1.5 +/- 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 (microU/ml) was increased after DPT, (18.0 +/- 3.0 vs. 11.5 +/- 1.2 (13), p = 0.04). Body temperature (degree C) was also significantly increased after DPT, (99.6 +/- 0.4 vs. 98.3 +/- 0.2 (14), p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)

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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 (%SB) 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 (%SB) 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 %SB 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 (*U/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 reductionin blood glucose. However, the elevation in plasma growth hormone cold buffer the hypoglycaemic effect of insulin, and help to maintain glucose homeostasis

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Red cell insulin binding was studied in 13 Jamaican children (age range 4-24 months), while malnourished (MAL), during early recovery (GI), late recovery (GII), and after anthropometric recovery (REC). The rate of weight gain (RW), the energy intake (EN), and the protein intake (PR) were monitored at each phase of the study. Four-hour fasting blood samples were used, and the insulin binding characteristics were investigated in the physiological range of insulin concentrations (16.7-1670 pM). Analyses of variance were used to examine differences in the variables measured at the four phases. Red cell-specific insulin binding (SB) was lower in MAL than in GI (P less than 0.001) and in (GII) (P = 0.026). SB in REC and MAL were not significantly different. Insulin receptor affinity (K) was also lower in MAL than in GI (P less than 0.001). GII (P = 0.001), and REC (P = 0.012). The insulin receptor number (S) appeared to be high in malnutrition and to decrease as recovery progressed; however the decrease was not significant. Children with fever demonstrated high insulin binding. Plasma insulin (IN) rose during recovery, and was significantly higher in GII than in MAL (P = 0.01). There was no difference in plasma glucose (G) at any phase of the study. The interrelationships among the variables measured were investigated longitudinally using multiple regression analyses, SB was positively associated with S (P = 0.032), EN (P = 0.029), and PR (P = 0.0076). S was negatively associated with K (P less than 0.001). The associations of S and K with PR were positive and approached significance (P = 0.09 and P = 0.07 respectively). RW was positively associated with PR (P less than 0.001), and with EN (P = 0.001). There were no significant relationships between G and any of the other variables longitudinally. However, correlations of the variables within phases demonstrated that in MAL, G was negatively associated with SB (P less than 0.05) and with K (P less than 0.05); but in REC, G was positively associated with SB (P less than 0.05). These results demonstrated that in severe malnutrition, the red cell insulin receptor affinity was low. During catch-up growth when protein and energy intakes were increased, both insulin receptor affinity and specific insulin binding were also increased. The negative relationship between insulin binding and plasma glucose during malnutrition may be related to carbohydrate intolerance.

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This study was designed to investigate any differences in cellular binding of insulin between phasic insulin-dependent (malnutrition-related) diabetes mellitus (PIDDM) and insulin-dependent, non-insulin-dependent, and normal controls. Isolated, washed red and white blood cells obtained after 12-14 hr fast, were separately incubated with varying concentrations of non-radioactive insulin, and a fixed quantity of radioactively labelled insulin. After the 3-hr incubation, cells were washed with buffer, and radioactivity determined on an autogamma counter. Percentage binding, receptor sites number and affinity were all determined by linear regression of the Scatchard plot. Fasting plasma insulin and glucose levels were also assayed. The results obtained show decreased binding of insulin in red blood cells [11.3 +/- 1.3%) and white blood cells 2.9 +/- 0.5%) in PIDDM. This was due to decreased receptor sites (red blood cells 39 +/- 11; white blood cells 0.5 +/- 0.11 x 10(4] as well as decreased affinity (red blood cells 0.14 +/- 0.03 x 10(9) M-1; white blood cells 0.17 +/- 0.04 x 10(9) M-1) when compared to the normal and diabetic (both insulin and non-insulin-dependent) controls. Phasic insulin-dependent diabetes (malnutrition-related diabetes mellitus) is characterized by decreased red and white cellular binding to insulin, in addition to decreased production of insulin.

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This study was designed to investigate any diferences in cellular binding of insulin between phasic insulin-dependent (malnutrition-related) diabetes mellitus (PIDDM) and insulin-dependent, non-insulin-dependent, and normal controls. Isolated, washed red and white blood cells obtained after 12 - 14hr fast, were separately incubated with varying concentrations of non-radioactive insulin, and a fixed quantity of radioactively labellede insulin. After the 3hr incubation, cells were washed with buffer, and radioactivity determined on an autogamma counter. Percentage binding, receptor sites number and affinity were all determined by linear regression of the Scathard plot. Fasting plasma insulin and glucose levels were were also assayed. The results obtained showed decreased binding of insulin in red blood cells (11.3+or -1.3%) and white blood cells 2.9 + or -o.5%) in PIDDM. This was due to decreased receptor sites (red blood cells 39+ or -11; white blood cells 0.5+ or -0.11x 10 to the 4th) as well as decreased affinity (red blood cells 0.14+ or -0.03 x 10 to the 9th M-1; white blood cells 0.17 + or -0.04 x10 to the 9th M-1) when compared to the normal and diabetic (both insulin and non-insulin-dependent) controls. Phasic insulin-dependent diabetes (malnutition-related diabetes mellitus) is characterized by decreased red and white cellular binding to insiulin, in addition to decreased production of insulin

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Plasma concentrations of free triiodothyronine (FT3), total triiodothyronine (TT3) and total thyroxine (TT4) were reduced to 63.0, 37.7, 61.7 per cent of controls respectively in protein-energy malnutrition (PEM), while free thyroxine (FT4) was elevated by 23 per cent. There was a gradual increase of both TT4 and TT3 during recovery. The ratio of free to bound hormones was high in malnutrition and declined with recovery, indicating a deficiency of thyroid-hormone binding in malnutrition. The observation of a significant reduction (P less than 0.05) in T3/T4 ratios, which occurred in malnutrition and was induced during recovery after 3 d on a low energy maintenance diet, suggested depressed conversion of T4 to T3 due to energy restriction. Energy restriction also significantly (P less than 0.001) depressed plasma insulin concentrations in the presence of nearly constant plasma glucose levels.

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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 104 +/- 11 (n = 20) pg/ml (mean +/- S.E.) significantly lower than during recovery when the maximum value was 180 +/- 24 (n = 13) pg/ml during the later recovery phase. After clinical recovery glucagon levels declined to 127 +/- 13 (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.

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The prevalence of rheumatoid arthritis has been compared in eight population samples in America and Europe, in which routine x rays were taken of the hands and feet. All the x rays were read by one observer. No relationship to lattitude was discovered. The prevalence of "definite" arthritis was not significantly different in the three racial groups included in these surveys, but "probable" disease was more common in the Negro population in Jamaica than in the Amerindians or Caucasians. Radiological evidence of erosive arthritis was more frequent in the Jamaican than in the Amerindian, and the Amerindian than the Caucasian. Serological tests for rheumatoid factor were more often positive in the Amerindian and erosive changes more severe. The implications of these findings are discussed.(Summary)

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