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Biomedical subjects

R H Fiser

Publications and source records attributed to R H Fiser.

At least 37 records · Page 2Linked to original sources
PubMed1977

Rare occurrence of Addison's disease and diabetes mellitus in children.

We report on two children with both Addison's disease and diabetes mellitus, a rare occurrence in children. One of the children first developed Addison's disease and later developed diabetes mellitus, while the other had the onset of diabetes mellitus first and later Addison's disease. In the latter patient a direct relationship was shown between the insulin dose and adrenal cortical hormone. Organ-specific antibody studies are reported and the diagnosis and management of these combined endocrinopathies are discussed.

Addison Disease↗
PubMed1976

Effects of fasting and theophylline on alanine-stimulated glucagon secretion in neonatal and infant sheep.

Plasma concentrations of glucose, alanine, and glucagon were measured after 24 hour fasting in newborn and infant sheep and in response to infusion of alanine alone and concurrently with theophylline. The plasma glucagon response to alanine was minimal in newborn sheep; in contrast, alanine produced a brisk response in plasma glucagon concentration in infant sheep. Glucose concentrations were unchanged in both groups. Theophylline enhanced blood glucagon and glucose responses to alanine in newborn animals but had minimal effects on the response of the infant sheep. These data, considered with earlier data in fetal sheep, suggest a progressive maturation of pancreatic islet alpha-cell glucagon secretion in the sheep during the postnatal period and suggest that the blunted glucagon response observed in the neonate is related to immaturity of the glucagon secretion mechanisms rather than deficient synthesis of the hormone. This immaturity may be related to impaired synthesis and/or enhanced degradation of cyclic adenosine monophosphate (cAMP) or to diminished responsiveness to cAMP.

Alanine↗
PubMed1975

Effects of oral alanine feeding on blood glucose, plasma glucagon and insulin concentrations in small-for-gestational-age infants.

The effects of oral alanine feeding on glucose homeostasis were evaluated in 21 infants who were small for gestational age and 26 who were appropriate for gestational age. In the first 24 hours, basal plasma alanine concentrations were higher in the former. Oral alanine feedings produced a significant rise over baseline levels of plasma alanine and glucagon concentrations in both groups. The blood glucose and plasma insulin concentrations also increased significantly in infants who were appropriate but not in those who were small for gestational age. At 25 to 96 hours of age, plasma glucagon, insulin and blood glucose concentrations did not change after the alanine feeding in either group. These data indicate that in the normally nourished infant (appropriate forgestational age), gluconeogenic amino acid (alanine) enhances hepatic glucose output. This phenomenon is not observed in the mainourished infants (small for gestational age), a point that may reflect decreased glycogen stores and ineffective gluconeogenic enzyme system in such infants.

Administration, Oral↗
PubMed1975

The effect of oral alanine on blood glucose and glucagon in the human newborn infant.

Plasma glucose, glucagon, and insulin responses to oral feedings of L-alanine were assessed in 44 healthy term infants during the first three days of life. Alanine administration produced significant increases in glucagon and glucose concentrations on day 1, but not on days 2 and 3. These increases occurred within 30 minutes (mean and SEM for glucagon, 127 plus or minus 7 to 219 plus or minus 16 pg/ml, P smaller than 0.001; glucose, 45 plus or minus 3 to 60 plus or minus 7 mg/100 ml, P smaller than 0.01) and persisted at the P smaller than 0.05 level at four hours. Responsiveness to alanine seemed to be related to the baseline blood glucose levels since constant infusions of glucose inhibited the response; These results indicate that the pancreatic islet alpha cell secretion mechanism(s) is functioning in the newborn.

Administration, Oral↗
PubMed1974

Spontaneous and amino acid-stimulated glucagon secretion in the immediate postnatal period. Relation to glucose and insulin.

The extent and significance of spontaneous glucagon secretion in the immediate postnatal period were investigated in groups of normal infants studied cross-sectionally and longitudinally. Arginine-and alanine-stimulated glucagon secretion was also studied. Plasma glucagon concentrations were correlated with prevailing glucose and insulin concentrations. The characteristic fall in blood glucose, reaching a nadir within hours of birth, was associated with a significant increase in glucagon concentration. Despite persistence of relative glucopenia, glucagon did not change appreciably between 2 and 24 h of life. A further significant elevation in glucagon concentration occurred from day 1 to day 3 of life associated with a return of glucose to euglycemic levels. In contrast to the sluggishness of pancreatic glucagon release, glucagon-like immunoreactivity rose markedly to mean levels of approximately 2,000 pg/ml after introduction of formula feeding. No significant changes in insulin levels were observed in these studies. Arginine infusion via an umbilical vein catheter into six infants within 6 h of birth elicited a brisk, almost threefold increment in glucagon concentration (from 339+/-85 to 940+/-254 pg/ml) in blood obtained from, or close to, the portal circulation. Bolus injection of alanine (1 mmol/kg) into a peripheral vein to six infants resulted in significant increments in glucagon (mean maximal, 128 pg/ml) as well as glucose and insulin. The observations suggest that spontaneous glucagon secretion may be an important factor in neonatal glucose homeostasis. Secretion seems more brisk in response to amino acid stimulation than to a falling glucose concentration.

Alanine↗