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Biomedical subjects

G Boden

Publications and source records attributed to G Boden.

At least 163 records · Page 9Linked to original sources
PubMed1976

Managing insulin-dependent diabetic patients.

About 95% of insulin-dependent diabetics can be managed satisfactorily with one or a combination of the follwoing insulin preparations: single-peak U-100 beef-pork NPH, Lente, and Regular. Complications of insulin therapy are commonly attributable to poor regulation of insulin dosage, irregular or excessive food intake, or unusual physical activity. One form of hyperglycemia is induced by insulin. Generalized allergic reactions to insulin sometimes require desensitization. Insulin-resistant patients are treated with a glucocorticoid.

Ambulatory Care↗
PubMed1975

Somatostatin suppresses secretin and pancreatic exocrine secretion.

Somatostatin, a hypothalamic peptide, suppresses hydrochloric acid-stimulated release of secretin, pancreatic flow rate, and bicarbonate and protein secretion in fasted, conscious dogs. It also reduces nonstimulated pancreatic exocrine secretion but does not affect basal secretin concentrations. Suppression of HCl-stimulated secretin release is complete, whereas pancreatic flow rate and bicarbonate and protein secretions are only partially inhibited. The action of somatostatin is rapid in onset and quickly reversible.

Animals↗
PubMed1975

Reversibility of pyloric sphincter dysfunction in gastric ulcer.

To investigate both the cause and reversibility of pyloric sphincter dysfunction in patients with gastric ulcer, pyloric sphincter pressures were measured in 10 normal subjects and 13 patients with gastric ulcer before and during gastric acidification. Fasting serum gastrin concentration was significantly higher in patients with gastric ulcer than in normal subjects. Compared to normals, patients with gastric ulcer had significantly lower pyloric pressures in response to intraduodenal amino acids and sodium oleate. However, during gastric acidification, these same patients demonstrated normal pyloric responses to these stimuli. Serum gastrin concentrations did not change during gastric acidification. These studies show that: (1) in patients with gastric ulcer the pyloric sphincter does not respond normally to intraduodenal stimulation; (2) fasting serum gastrin concentration is elevated in patients with gastric ulcer; and (3) in these patients, pyloric sphincter dysfunction can be reversed by gastric acidification. The mechanism of pyloric dysfunction in patients with gastric ulcer remains unknown.

Adult↗
PubMed1974

Effects of intraduodenal administration of HCl and glucose on circulating immunoreactive secretin and insulin concentrations.

A new radioimmunoassay for secretin was used to investigate (a) serum secretin responses to intraduodenally infused HCl and glucose, (b) the metabolic half-life and the volume of distribution of exogenous secretin and (c) the effect of endogenously released secretin on insulin secretion in 25 anesthetized dogs. Portal and femoral venous blood samples were taken simultaneously before, during, and after intraduodenal infusion of HCl (21 meq/30 min) and glucose (131 ml/30 min). Control experiments were performed with intraduodenal infusion of saline. Mean portal venous immunoreactive secretin concentration of six dogs rose from 313 muU/ml before to 1,060 muU/ml 10 min after initiation of the intestinal acidification (P < 0.005). Femoral venous immunoreactive secretin concentration rose from 220 muU/ml before to 567 muU/ml 15 min after intestinal acidification (P < 0.01). Secretin concentrations remained elevated during the remainder of the infusion. In the same six dogs mean portal venous immunoreactive insulin concentration rose from 38 muU/ml before to 62 muU/ml at the end of the infusion (P < 0.05). Peripheral immunoreactive insulin, glucose, and free fatty acid concentrations, however, did not change significantly. Pancreatic exocrine function was studied in four dogs. The rise in secretin concentration was followed promptly by a highly significant increase in exocrine pancreatic flow rate and bicarbonate secretion, indicating biological activity of the circulating immunoreactive secretin. The effect of intraduodenal infusion of glucose on immunoreactive secretin concentration was studied in 12 dogs. Glucose in concentrations ranging from 2.5% to 10% had no detectable influence on portal or peripheral secretin concentration. Infusion of 50% glucose caused a slight decline in secretin concentration. The metabolic clearance rate, half-life of disappearance, and volume of distribution of exogenous secretin was studied in three dogs by the constant infusion technic. The metabolic clearance rate was 730+/-34 ml/min, volume of distribution was 17.4+/-0.8% of body weight, and the half-life of disappearance was 2.8+/-0.1 min. It could be calculated that 1.38 U/kg-h(-1) of endogenous secretin was released into the peripheral circulation during the steady state period of the HCl infusion experiments. The data indicated that immunoreactive secretin was released rapidly after intestinal acidification, continued to be secreted throughout the duration of HCl infusion, and was promptly distributed in the extracellular compartment. Furthermore, they suggested that endogenously released secretin could stimulate insulin secretion. The HCl-mediated insulinogenic effect of immunoreactive secretin, however, was too weak to influence peripheral immunoreactive insulin, glucose, and free fatty acid concentrations. The failure of intraduodenal glucose to stimulate secretin release suggests that secretin is not the insulin-stimulatory factor released from the gastrointestinal tract in response to glucose.

Animals↗
PubMed1974

Hepatic ketogenesis and gluconeogenesis in humans.

Splanchnic arterio-hepatic venous differences for a variety of substrates associated with carbohydrate and lipid metabolism were determined simultaneously with hepatic blood flow in five patients after 3 days of starvation. Despite the relative predominance of circulating beta-hydroxybutyrate, the splanchnic productions of both beta-hydroxybutyrate and acetoacetate were approximately equal, totaling 115 g/24 h. This rate of hepatic ketogenesis was as great as that noted previously after 5-6 wk of starvation. Since the degree of hyperketonemia was about threefold greater after 5-6 wk of starvation, it seems likely that the rate of ketone-body removal by peripheral tissues is as important in the development of the increased ketone-body concentrations observed after prolonged starvation as increased hepatic ketone-body production rate. Splanchnic glucose release in this study was 123 g/24 h, which was less than that noted previously after an overnight fast, but was considerably more than that noted during prolonged starvation. Hepatic gluconeogenesis was estimated to be 99 g/24 h, calculated as the sum of lactate, pyruvate, glycerol, and amino acid uptake. This was greater than that observed either after an overnight fast or after prolonged starvation. In addition, a direct relationship between the processes of hepatic ketogenesis and gluconeogenesis was observed.

Acetoacetates↗
PubMed1973

Rapid intravenous sodium acetoacetate infusion in man. Metabolic and kinetic responses.

The metabolic and kinetic responses to rapidly intravenously administered sodium acetoacetate (1.0 mmol/kg body wt) was studied after an overnight fast in 12 male and female adults weighing between 88 and 215% of average body weight. Blood was obtained before, during, and after the infusion for determination of circulating concentrations of immunoreactive insulin, glucose, acetoacetate, beta-hydroxybutyrate and free fatty acids. In three obese subjects the studies were repeated after 3 and 24 days of total starvation. After the overnight fast acetoacetate rose rapidly reaching a peak concentration at the end of the infusion; beta-hydroxybutyrate concentrations also increased rapidly and exceeded those of acetoacetate 10 min postinfusion. Total ketone body concentration at the end of the infusion period was comparable to that found after prolonged starvation. After the initial mixing period, acetoacetate, beta-hydroxybutyrate and total ketone bodies rapidly declined in a parallel manner. There were no obvious differences between the subjects with regard to their blood concentrations of ketone bodies. The mean plasma free fatty acid concentration decreased significantly during the 20th to 90th min postinfusion period; for example the control concentration of 0.61 mmol/liter fell to 0.43 mmol/liter at 60 min. In the three obese subjects studied repeatedly, fasting plasma free fatty acids decreased with acetoacetate infusion from 0.92 to 0.46 mmol/liter after the 3 day fast and from 1.49 to 0.71 mmol/liter after the 24 day fast. Acetoacetate infusion caused no changes in blood glucose concentration after an overnight fast. However, in the three obese subjects restudied after 3- and 24-day fasts blood glucose decreased, respectively, from 3.49 to 3.22 mmol/liter and from 4.07 to 3.49 mmol/liter. The mean serum insulin concentration in all subjects significantly increased from 21 to 46 muU/ml at the completion of the infusion and rapidly declined. In the three obese subjects restudied after 3- and 24-day fasts an approximate two-fold increase of serum insulin was observed after each acetoacetate infusion. The mean fractional utilization rate of exogenously derived ketone bodies for all 12 subjects after an overnight fast was 2.9% min(-1). In the three obese subjects studied after an overnight, 3 and 24 day fast the mean fractional utilization rates were 2.1%, 1.5%, and 0.6% min(-1), respectively. Ketone body volumes of distribution in the overnight fasted subjected varied from about 18% to 31% of body wt, suggesting that ketone bodies are not homogenously distributed in the body water. In the three obese subjects restudied after 3- and 24-day fasts volumes of distribution remained approximately constant. When total ketone body concentrations in the blood were below 2.0 mmol/liter, there was a linear relationship between ketone body utilization rates and ketone body concentrations; no correlation was found when blood concentrations were higher.

Acetoacetates↗
PubMed1972

The effect of carbohydrates on ammonium and ketoacid excretion during starvation.

The metabolic effects of oral ingestion of minute quantities of carbohydrate during prolonged starvation were studied in nine obese subjects. Measurements were made during a control period of total starvation, during the ingestion of 7.5 g carbohydrate daily, and finally during the ingestion of 15.0 g carbohydrate daily. Daily ketoacid excretion fell after carbohydrate ingestion and was significantly correlated (r = 0.62, P < 0.01) with the amount of carbohydrate administered. Despite this fall in ketoacids, the concentration of blood ketoacids, plasma free fatty acids, and serum insulin remained constant throughout the study. Urinary ammonium excretion, closely correlated with ketoacid output (r = 0.95, P < 0.001), also fell significantly after carbohydrate ingestion. No significant changes were present in extracellular or urinary pH. Urea nitrogen excretion did not change when urinary ammonium output fell. These results indicate that: the excretion of ketoacids and ammonium in starving man is exquisitely sensitive to minute amounts of ingested carbohydrate; the change in ketonuria appears to be due to increased renal ketoacid reabsorption after carbohydrate ingestion; and the nitrogen-sparing effect of reducing renal ammonium output in starvation can be dissociated from nitrogen sparing occurring because of changes in urine urea excretion.

Adolescent↗