Hazel M Robinson

Glucose tolerance and insulin sensitivity in malnourished children.

I . In malnourished, compared with recovered children, fasting blood glucose concentrations were low and there was impaired peripheral glycolysis as shown by a failure of blood lactate to rise after glucose was injected intravenously. 2. Homogenates of muscle biopsies from malnourished and recovered children produced equal amounts of lactate when incubated anaerobically with various substrates, but when compared with homogenates of biopsies from normal children the pattern suggested an impairment of glycolysis. 3. The rate of glucose disappearance after intravenous glucose was slow in the malnourished child and there was possibly diminished sensitivity to exogenous insulin. 4, Isocaloric diets relatively high or low in fat were fed to children who had recovered from malnutrition. Glucose tolerance, insulin sensitivity, fasting plasma insulin and insulin response to intravenous glucose were all the same in children on either diet.

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

Summary: 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 μU/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 malnutrition and was significantly decreased to normal levels after

Effects of cassava cyanoglucoside, linamarin, on blood sugar levels in the dog

Abstract This study was undertaken to examine the diabetogenicity of linamarin in dogs of different nutritional status. The total dog population was 35; 15 normals, 10 undernourished, and 10 recovered. The recovered dogs were the refed undernourished dogs. On each dog a fasting plasma insulin and insulin receptor studies were done, followed by a controlled glucose tolerance test. After feeding linamarin, 0.5 hour was allowed to elapse before these investigations were repeated. In the linamarin-treated undernourished animal, plasma insulin and insulin binding to erythrocytes and mononuclear leucocytes were significantly (P

Fasting Pancreatic Glucagon in Jamaican Children during Malnutrition and Subsequent Recovery

Summary: 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.Speculation: Low pancreatic glucagon and insulin levels in protein energy malnutrition are adaptive mechanisms to conserve tissue by reducing anabolic and catabolic processes. The increases in hormone concentrations during recovery reflect the increased metabolism associated with growth, and the anabolic actions of insulin dominates glucagon action to promote new tissue synthesis and dramatic increases in weight gain.

NORMAL, PRODUCTION AND INCREASED OXIDATION OF GLUCOSE ASSOCIATED WITH EPINEPHRINE DEFICIENCY IN “KETOTIC” HYPOGLYCEMIA

Neither the current hypothesis that “ketotic” hypoglycemia results from deficient gluconeogenesis nor the alternative of increased glucose oxidation has been adequately tested. Three affected children (H) were compared with their unaffected identical twins (C) while fasting until hypoglycemic or nearly glycogen depleted. Plasma glucose production (flux, measured by constant infusion of 13C-glucose) was the same earlier in the fast during glycogenolysis (H = 19, C = 19 μmoles/min/kg), as well as later when it was derived almost entirely from gluconeogenesis (H = 15, C = 16 μmoles/min/kg). Potentially available glycerol or amino acids for gluconeogenesis (determined from respiratory calorimetry and N excretion) were not less in H (alanine was lower). However, glucose oxidation (by calorimetry) was greater in H while glucose fell rapidly preceding symptoms (H = 17, C = 8 μmoles/min/kg). Urine epinephrine rose in C as glucose fell, but not in H until after becoming hypoglycemic and the maximum was much less (H = 0.6, C = 1.6 ng/min/kg). There was also a delayed rise in plasma lipolysis products and failure to suppress insulin in H. Inhibition of glyoolysis by infusion of 2-deoxyglucose raised epinephrine, glucose, and FFA in C, but not in H. In conclusion, acquired epinephrine deficiency can account for this impaired transition from glucose bo fat oxidation resulting in hypoglycemia.