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Biomedical subjects

M A Sperling

Publications and source records attributed to M A Sperling.

At least 91 records · Page 5Linked to original sources
PubMed1979

Blunting of spontaneous and alanine-stimulated glucagon secretion in newborn infants of diabetic mothers.

Spontaneous and alanine-stimulated glucagon secretion, and its relation to plasma glucose concentration was investigated in two groups of infants during the initial two hours of life. At birth, plasma glucagon and glucose concentrations were not significantly different in healthy term newborn infants (control subjects) and infants born to insulin-dependent diabetic mothers(IDM-l). In control infants during the first hour of life, glucose fell by 43 +/- 16 mg per deciliter (mean +/- S.E.M.) while plasma glucagon rose by 44 +/- 16 pg. per milliliter (p less than 0.05 for both). However, in IDM-I despite a fall in glucose greater than in control infants, plasma glucagon failed to significantly increase. Intravenous alanine, 150 mg. per kilogram, given at one hour of life, elicited significant increments in glucose and glucagon which were positively correlated in control infants. No significant change in glucose or glucagon occurred in the diabetic group. None of the control infants developed symptomatic or biochemical hypoglycemia (plasma glucose less than 20 mg. per deciliter) whereas five of ten IDM-I developed hypoglycemia. These results suggest that spontaneous and alanine-stimulated glucagon secretion is obtunded in IDM and that this may contribute to hypoglycemia in these infants.

Alanine↗
PubMed1979

Bidirectional placental transfer of glucose and its turnover in fetal and maternal sheep.

Glucose biokinetics were assessed simultaneously in the pregnant ewe and its fetus by a primed constant infusion of 2-3H glucose and U-14C glucose. Late in gestation fetal glucose turnover was 27.3 +/- 3.7 mg/min; expressed in terms of fetal weight this is 6 to 10 mg/kg/min. In the fed state the results indicated that all of the fetal glucose turnover was derived from the mother via placental transfer and there was no evidence that the fetus was capable of glucose production. Maternal glucose turnover was 145.6 +/- 9.3 mg/min (2.8 mg/kg/min). There was a significant amount of glucose (16.3 +/- 2.3 mg/min) transferred from the fetus to the mother. This feto-maternal transfer of glucose accounted for 11% of the maternal glucose turnover and approximately 50% of the total glucose coming to the fetus from the mother. This study provides the first in vivo simultaneous quantification of the bidirectional glucose transfer across the placenta.

Animals↗
PubMed1977

The contribution of hyperglycemic hormones to the pathogenesis of diabetes mellitus.

Changes in cortisol, growth hormone, and glucagon levels observed in diabetes mellitus appear to be secondary to insulin deficiency, and can be related to the severity of insulinopenia with its attendant metabolic sequelae. Similarly, disturbances in plasma concentrations of catecholamines in diabetes also appear to be secondary to insulin deficiency, although a primary disturbance in adrenergic function or receptors at the cellular level cannot be excluded. As "inappropriate" compensatory responses, these hormones may aggravate the diabetic syndrome, but their dysfunction is not the cause of diabetes and cannot be used to identify prediabetes. To date, the primary hormonal disturbance in insulin-dependent diabetes remains defective insulin secretion.

Diabetes Mellitus↗
PubMed1977

Does glucagon play a role in the insulin resistance of patients with adult non-ketotic diabetes?

Using a constant intravenous infusion technique we have measured in vivo insulin resistance in 17 normal subjects, five patients with chemical diabetes, and 13 non-ketotic diabetic patients with fasting hyperglycaemia (FBS greater than 120 mg/100 ml). All of the diabetic patients were non-obese. The results demonstrated that the diabetic patients were insulin resistant compared to normals and that the degree of insulin resistance was greater the more severe the diabetes. No differences in plasma glucagon levels were found among the different groups during the infusion studies. These results demonstrate that non-obese, non-ketotic diabetic patients are insulin resistant and that abnormalities in plasma glucagon concentrations do not account for this insulin resistance.

Adult↗
PubMed1977

Suppressibility of glucagon secretion by glucose in juvenile diabetes.

The suppressibility of plasma glucagon concentrations by glucose was investigated in normal and diabetic children. Fasting concentrations of plasma glucagon were similar in normal and in diabetic children despite the hyperglycemia of the latter. Infusion of glucose promptly suppressed glucagon values in the normal as well as in the diabetic children pretreated with half of their usual morning dose of insulin. Glucose alone, however, did not suppress plasma glucagon in diabetic patients, despite the attainment of significant hyperglycemia. Administration of insulin during an ongoing glucose infusion in the diabetic patients lowered their blood glucose concentration; the concentration of glucagon rose transiently when the glucose concentration fell. These data confirm the existence of relative hyperglucagonemia inappropriate for the degree of blood glucose concentration in diabetic children deprived of insulin. The data also suggest that this hyperglucagonemia is secondary to insulin deficiency and suppressibility of glucagon by glucose can be restored by insulin therapy.

Adolescent↗
PubMed1977

Pancreatic alpha and beta cell functions in cystic fibrosis.

Insulin and glucagon secretions were studied during oral glucose tolerance testing and arginine infusion in 13 patients with cystic fibrosis. Two groups of patients were identified; Group I (N=6) whose OGTT was entirely normal and Group II (N=7) who had some abnormality in glucose during OGTT. In each group basal glucagon concentrations were normal and supressed appropriately (p less than 0.05) after glucose; insulin responses were attenuated and the peak responses delayed. During arginine stimulation, insulin secretion was impaired in each group. However, glucagon secretion was diminished only in Group II. Thus, insulinopenia was found in both groups and hyperglucagonemia was not found as a contributory factor to the hyperglycemia in Group II.

Adolescent↗
PubMed1977

Intestinal adaptation after jejunoileal bypass in man.

Gastrointestinal anatomy and function has been studied prospectively in 12 patients undergoing jejunoileal bypass surgery in order to investigate the adaptive response of the intestinal mucosa. The total thickness of the jejunal mucosa did not change after surgery, but the crypts became relatively deeper, suggesting a more rapid turnover of gastrointestinal cells. The absorption of oxalate was depressed in the immediate postoperative period but had improved toward preoperative levels by 6 months. Vitamin B12 absorption also declined postoperatively, and increased thereafter in the patients with an end-to-end jejunoileostomy, but showed a much smaller recovery in the group with an end-to-side anastomosis. The cholesterol concentration (lithogenicity) of the duodenal bile rose by 30% in the first 3 weeks after surgery, but had returned to preoperative levels by 6 months. The segmental absorption of glucose across the jejunum declined after surgery. Caloric intake also declined, whether measured as the quantity of food that patients elected to eat over a 24-hr period, or as the quantity of a liquid lunch which they consumed over a 20-min period. The level of basal gastric acid was increased postoperatively but the maximal output after histamine stimulation was not. The gastrin response to a standard liquid meal was also significantly increased after surgery. Enteroglucagon secretion showed an increase in 3 weeks and a further increase by 6 months after intestinal bypass surgery. The significance of these changes to intestinal adaptations is discussed.

Bile Acids and Salts↗
PubMed1977

Possible mechanisms and significance of the neonatal surge in glucagon secretion: studies in newborn lambs.

Studies were conducted in newborn lambs to gain insight into the significance and mechanism(s) responsible for the rapid rise in plasma immunoreactive glucagon (IRG) which occurs in human and other newborn species immediately after delivery. Three sets of experiments were conducted: group A, control studies (n = 5) in which delivery into room air was followed 1 hr later by cutting of the umbilical cord and periodic blood sampling for a further hour; group B, studies (n = 5) in which somatostatin (SRIF), a known inhibitor of IRG and insulin (IRI) secretion, was infused int othe fetus for 10 min before, and for 1 hr after delivery and immediate cord cutting; group C, studies (n = 5) in which an identical dose regimen of SRIF was infused into fasting newborn lambs aged 24-72 hr. The doses of SRIF used were several fold higher than those proven to suppres pancreatic hormones secretion in other species. In the control studies, plasma IRG levels remained stable until the cord was cut, after which event levels rose 5-6-fold (59 +/- 15 pg/ml to 305 +/- 98 pg/ml, P less than 0.05). Simultaneously, plasma free fatty acid (FFA) concentrations rose significantly (280 +/- 80 to 780 +/- 100 muEq/liter, P less than 0.05) and IRI remained unchanged. Plasma glucose concentrations, however, in contrast to observations in other species, did not fall, and therefore, hypoglycemia was not the stimulus for the glucagon surge. SRIF infusion at birth (group B) did not prevent the rise in IRG. Again blood glucose values did not fall, but in contrast to the control studies plasma IRI levels rose and the rise in FFA did not occur. Later SRIF infusion (group C) resulted a prompt and sustained suppression of IRG and IRI and a significant fall in blood glucose. These results suggest that an adrenergic mechanism rather than curtailment of nutrients is the major stimulus to the neonatal surge in IRG.

Animals↗
PubMed1977

Measurement of "true" glucose production rates in infancy and childhood with 6,6-dideuteroglucose.

"New" glucose production has been measured in 54 infants and children for the first time by continuous three-to-four-hour influsion of the safe, nonradioactive tracer 6,6-dideuteroglucose. The use of combined gas chromatography--mass spectrometry with monitoring of selected ions allowed deuterium enrichment in blood glucose to be measured on microliter samples with an error of less than 2 per cent. In the young child, glucose production increased in a slightly curvilinear manner from 1 kg. to 25 kg. body weight, when it reached 140 mg. per minute, almost the adult value of 173 mg. per minute (2.28 +/- 0.23 mg./kg.-min., mean +/- S.E.). Normalized for weight, glucose production in premature infants was 5.46 +/- 0.31 mg./kg.-min., in term neonates averaged 6.07 +/- 0.27 mg./kg.-min., in children below the age of six years was 7.1 +/- 0.27 mg./kg.-min., and in late childhood averaged 5.4 +/- 0.28 mg./kg.-min. Relative to estimated brain weight, however, glucose production was essentially linear from the 1-kg. premature infant to the 80-kg. adult. These data, the first measurements of "new" glucose production in childhood, suggest that brain size may be a principal determinant of those factors that regulate hepatic glucose output throughout life.

Blood Glucose↗
PubMed1977

Low-dose continuous insulin therapy for diabetic ketoacidosis. Prospective comparison with "conventional" insulin therapy.

Low-dose insulin infusion has recently been used to treat ketoacidosis. We have prospectively compared patients with ketoacidosis either treated with insulin infusion at the rate of 6 units per hour or with high-dose, intermittent subcutaneously administered insulin, with emphasis placed on the hormonal responses. Basal glucagon, cortisol, and growth hormone levels were elevated in both groups. Cortisol and growth hormone levels did not fall with therapy in either group but glucagon levels fell in parallel with glucose levels in both groups. There was no difference in the time taken for glucose levels to fall below 250 mg/100 ml between groups. Whereas both methods of therapy appeared to be equally effective, low-dose infusion had the advantages of ease of administration, a predictable, relatively linear rate of fall of glucose levels, and ability to be stopped abruptly in the event of hypoglycemia.

Blood Glucose↗
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↗