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Biomedical subjects

G Boden

Publications and source records attributed to G Boden.

At least 145 records · Page 8Linked to original sources
PubMed1980

Monitoring metabolic control in diabetic outpatients with glycosylated hemoglobin.

The usefulness of HbA, as a monitor of metabolic control was studied in 15 diabetic outpatients during periods of stable, deteriorating, and improving control. Mean fasting concentrations of HbA, and plasma glucose during a 3-month period of stable control were 12.6% +/- 0.8% and 120 +/- 8 mg/dL, respectively. One week after discontinuation of oral hypoglycemic therapy, blood glucose had risen to 172 +/- 23 mg/dL and HbA, to 14.1% +/- 0.7% (P less than 0.025). Reinstitution of therapy resulted in a significant fall of blood glucose within 2 weeks. A significant decline in HbA1 (from 15.3% +/- 0.8% to 14.1% +/- 0.9%, P less than 0.025) occurred 2 weeks later. The data show that the rate of formation of HbA1 is considerably faster than its rate of disappearance. Thus, HbA1 is likely to reflect disproportionally recent episodes of poor control. We conclude that HbA1 is useful to monitor diabetic outpatients during periods of stable and rapidly deteriorating control but is not suited to detect rapid metabolic improvements.

Administration, Oral↗
PubMed1979

Energy metabolism in feasting and fasting.

During feasting on a balanced carbohydrate, fat, and protein meal resting metabolic rate, body temperature and respiratory quotient all increase. The dietary components are utilized to replenish and augment glycogen and fat stores in the body. Excessive carbohydrate is also converted to lipid in the liver and stored along with the excessive lipids of dietary origin as triglycerides in adipose tissue, the major fuel storage depot. Amino acids in excess of those needed for protein synthesis are preferentially catabolized over glucose and fat for energy production. This occurs because there are no significant storage sites for amino acids or proteins, and the accumulation of nitrogenous compounds is ill tolerated. During fasting, adipose tissue, muscle, liver, and kidneys work in concert to supply, to convert, and to conserve fuels for the body. During the brief postabsorptive period, blood fuel homeostasis is maintained primarily by hepatic glycogenolysis and adipose tissue lipolysis. As fasting progresses, muscle proteolysis supplies glycogenic amino acids for heightened hepatic gluconeogenesis for a short period of time. After about three days of starvation, the metabolic profile is set to conserve protein and to supply greater quantities of alternate fuels. In particular, free fatty acids and ketone bodies are utilized to maintain energy needs. The ability of the kidney to conserve ketone bodies prevents the loss of large quantities of these valuable fuels in the urine. This delicate interplay among liver, muscle, kidney, and adipose tissue maintains blood fuel homeostasis and allows humans to survive caloric deprivation for extended periods.

Acid-Base Equilibrium↗
PubMed1979

Effects of endogenous hyperglucagonemia on lower esophageal sphincter pressure and gastric acid secretion.

Lower esophageal sphincter function and gastric acid secretion were studied in a patient with endogenous hyperglucagonemia due to a functioning islet cell carcinoma. Complete resection of the tumor resulted in a fall of the serum concentration of immunoreactive glucagon to a normal level. Pre- and postoperative resting lower esophageal sphincter pressures and lower esophageal sphincter pressure responses to administration of pentagastrin, edrophonium, and bethanechol were unchanged. After surgery, preoperative immunoreactive glucagon concentrations were reproduced by intravenous infusion or intramuscular injection of exogenous glucagon. Lower esophageal sphincter resting pressures and responses to agonists were unchanged. In contrast, glucagon administered at 36 micrograms/kg/hr, which produced a serum concentration of immunoreactive glucagon (32,000 pg/ml) much greater than observed preoperatively (1200 pg/ml), diminished resting lower esophageal sphincter pressure and sphincter responses to pentagastrin, edrophonium, and bethanechol. Similarly, pentagastrin-stimulated gastric acid secretion was unaffected by tumor resection or low-dose glucagon infusion but was decreased at a glucagon infusion rate of 36 micrograms/kg/hr. This series of observations supports the thesis that endogenous glucagon plays no physiological role in the regulation of lower esophageal sphincter pressure or gastric acid secretion.

Adenoma, Islet Cell↗
PubMed1978

Effects of a protein meal, intraduodenal HCl, and oleic acid on portal and peripheral venous secretin and on pancreatic bicarbonate secretion.

We have studied the effect of a protein meal on secretin (IRS) concentration in dogs and humans using a radioimmunoassay of improved sensitivity (8 pg/ml). After a meal, pancreatic bicarbonate secretion (PBS) increased markedly and proximal duodenal pH decreased from 6.2 to 4.3. Portal and peripheral IRS concentrations, however, remained unchanged in eight dogs and five patients with cirrhosis of the liver. Similarly, an alkaline solution of sodium oleate (pH 9.2) stimulated PBS but not IRS. Intraduodenal administration of various amounts of HCl in dogs demonstrated that acid-stimulated PBS was invariably accompanied by rises in peripheral venous IRS concentration. We conclude that the postprandial stimulation of PBS involves mechanisms more complex than acid-stimulated secretin release.

Adult↗
PubMed1978

Pancreatic polypeptide responses to a meal and to intraduodenal amino acids and sodium oleate.

Serum concentrations of immunoreactive pancreatic polypeptide (IR-PP) were measured in dogs in response to a meal and to intraduodenal infusions of amino acids, Na oleate, and HCl. In addition, the effects of somatostatin on meal-stimulated IR-PP concentrations were studied. In response to a meal, IR-PP rose from 151 +/- 19 pg/ml to 296 +/- 35 pg/ml (P less than 0.01) at 15 min, reached a plateau of 367 +/- 56 pg/ml at 45 min, and remained elevated for 4 h. In response to intraduodenal amino acids, IR-PP rose from 196 +/- 22 pg/ml to 342 +/- 19 pg/ml (P less than 0.01), and serum alanine rose from 251 +/- 18 mM to 361 +/- 30 mM. Peak concentrations of IR-PP, however, were reached before alanine rose above baseline. During administration of intraduodenal Na oleate, IR-PP rose from 181 +/- 21 pg/ml to 348 +/- 17 pg/ml (P less than 0.01). Intraduodenal HCl had no effect on IR-PP. Intravenous somatostatin (100 microgram/h) suppressed meal-stimulated IR-PP from 450 +/- 68 pg/ml to 133 +/- 23 pg/ml (P less than 0.01). The data indicate 1) IR-PP is increased after a meal and intraduodenal administration of amino acids and Na oleate; 2) the increases in serum IR-PP precede increases in serum levels of absorbed alanine; and 3) somatostatin suppresses the meal-stimulated increase in serum IR-PP.

Amino Acids↗
PubMed1977

Familial hyperglucagonemia--an autosomal dominant disorder.

Basal immunoreactive glucagon was elevated in four of nine asymptomatic relatives of a patient with glucagonoma. Immunoreactive glucagon remained elevated throughout 22 to 25 hours of continuous observation. Glucagon responses to intravenous glucose and arginine or mixed meals (or both) were abnormal, whereas glucose and insulin responses were normal. Gel filtration of plasma revealed that over 85 per cent of the four relatives' immunoreactive glucagon had a molecular weight of greater than 9000 daltons whereas that of 70 per cent of the patients with glucagonoma had a molecular weight of 3500 daltons, with the remainder eluting in the area of 9000 daltons. Pancreatic angiograms and hepatic scintiscans were normal in all four relatives. The data suggest an autosomal dominant transmission of hyperglucagonemia in this family. Immunoreactive glucagon with a molecular weight of 3500 or 9000 daltons appears to be required for the development of the clinical glucagonoma syndrome.

Adenoma, Islet Cell↗
PubMed1977

Human splanchnic metabolism during diabetic ketoacidosis.

Splanchnic exchange rates of glucose, acetoacetate, beta-hydroxybutyrate, lactate, pyruvate, glycerol, alanine, glutamine, glutamate, free fatty acids, and triglycerides were measured in eight patients during moderate to severe diabetic ketoacidosis. Their arterial glucose concentration was 20.68 (9.80-52.79) mumole/liter and tic glucose release was 0.77 (0.09-2.44) mmole/min. Gluconeogenesis accounted for about one-half of net splanchnic glucose release, assuming quantitative conversion of net splanchnic extracted lactate, pyruvate, glycerol, alanine, and alpha-ketoglutarate equivalents to glucose. Net splanchnic free fatty acid extraction was 0.24 (0.09-0.52) mmole/min. There was a positive correlation between free fatty acid uptake and ketone-body release. Net splanchnic acetoacetate release was 0.50 (0.05-0.92) mmole/min and beta-hydroxybutyrate release was 0.35 (-0.16 to 0.84) mmole/min. Total ketone-body release was 0.84 (0.37-1.61) mmole/min. The wide ranges of net splanchnic glucose and ketone-body production rates show the heterogeneous characteristics of the diabetic patient in ketoacidosis. It is concluded that the hyperglycemia and hyperketonemia of diabetic ketoacidosis is due to the lack of reciprocity among rates of hepatic glycogenlysis, gluconeogenesis, and ketogenesis resulting in inappropriate net splanchnic release of glucose and ketone bodies.

Alanine↗
PubMed1977

Effect of somatostatin on meal-stimulated pancreatic exocrine secretions in dogs.

The effect of exogenously administered somatostatin (SRIF) on meal-stimulated secretions of the exocrine pancreas was studied in dogs with chronic pancreatic fistulas. Dogs were fed 600 gm. of raw meat, and pacreatic output of water, bicarbonate, and protein was measured. Bicarbonate and protein secretions rose markedly postfeeding in all control animals. Four hundred micrograms or 100 mug. of SRIF infused for one hour together with a meal completely prevented the postfeeding rise in pancreatic secretions. SRIF (100 mug./hr.) infused one hour after a meal suppressed pancreatic secretions to basal levels within 30 minutes. Pancreatic secretions rose promptly after discontinuation of SRIF in all dogs. These data indicate (1) SRIF completely prevents pancreatic bicarbonate and enzyme responses when given together with a meal; (2) it completely suppresses already initiated pancreatic responses when given one hour after a meal; (3) 100 mug. of SRIF is as effective as 400 mug. in suppressing the postprandial rise in pancreatic secretions. We conclude that SRIF severely interferes with pancreatic secretions during normal alimentation and that this observation should be considered if SRIF is to be used as a therapeutic agent.

Animals↗
PubMed1977

An islet cell carcinoma containing glucagon and insulin. Chronic glucagon excess and glucose homeostasis.

Described here is a patient who had an islet cell carcinoma containing both glucagon (glucagonoma) and insulin (insulinoma). Complete removal of the tumor was possible. Immunoreactive glucagon (IRG) could be extracted from all parts of the tumor (approximately 50 mug./gm.) and was shown to be fully bioactive. Immunoreactive insulin (IRI) could be extracted only from one section of the tumor (approximately 30 mug./gm.). The clinical and biochemical manifestations of the disease were dermatitis, diabetes, weight loss, anemia, hypoaminoacidemia, and hyperketonemia. The diabetes was characterized by low or normal fasting blood glucose concentrations and by impaired glucose tolerance (Kg = 0.4). After complete removal of the tumor, the dermatitis cleared, the catabolic state changed into an anabolic state, blood amino acid concentrations increased, and blood ketone-body concentrations decreased. Fasting blood glucose concentrations, however, rose above 200 mg./dl., and glucose tolerance declined further (Kg = 0.15). Hourly blood sampling for 24 hours, intravenous and oral glucose tolerance tests, intravenous arginine and tolbutamide tolerance tests with serial determinations of IRG, IRI, and blood glucose were performed preoperatively and again two weeks and two months postoperatively. The results of these studies demonstrated marked abnormalities in the stimulation and suppression of glucagon and insulin release. In addition, they failed to demonstrate a glycemic effect on the chronically elevated glucagon concentrations in this patient, while identifying insulin as the dominant factor determining blood glucose homeostasis.

Adenoma, Islet Cell↗
PubMed1977

A test of the hypothesis that the rate of fall in glucose concentration triggers counterregulatory hormonal responses in man.

The hypothesis that the rate of fall in glucose concentration triggers counterregulatory hormonal responses was tested in five subjects following one hour of sustained hyperglycemia. Despite a rapidly falling blood glucose concentration, no increase in plasma growth hormone, cortisol, glucagon, or catecholamines occurred as long as the blood glucose concentration remained above fasting levels. Plasma growth hormone, cortisol, and catecholamines were not released until the mean blood glucose reached 28 mg./100 ml., 39 mg./100 ml., and 39 mg./100 ml., respectively, below the fasting level. Plasma glucagon was suppressed during the period of hyperglycemia. As the blood glucose concentration fell below basal levels, a progressive increase in glucagon occurred. Plasma glucagon returned to fasting values when the nadir in blood glucose was attained. During the period of rapidly falling blood glucose, only plasma insulin showed any change; its response lagged behind the decline in blood glucose. By the time the fasting glucose level was attained, the plasma insulin was still almost three times the basal level. We concluded that under our experimental conditions the rate of fall in blood glucose and the degree of hypoglycemia achieved is primarily determined by the plasma insulin concentration.

Blood Glucose↗
PubMed1977

The role of some polar amino acid residues in secretin.

Three analogues of S5-27, the tricosapeptide with the carboxyl-terminal sequence of secretin, were studied. In the analogues, the acidic residues at positions 9 and 15 of S5-27 were replaced by the neutral residues glutamine and asparagine. These changes resulted in a decrease in immunoreactivity. Binding to an antibody against secretin could be correlated with the changes in the conformation of the synthetic analogues.

Amino Acid Sequence↗
PubMed1977

Bile-fat relationships in gastric secretory inhibition and bile flow stimulation.

The effect of intraduodenal infusion of olive oil, bile, or a mixture of olive oil and bile on pentagastrin-stimulated gastric secretion, bile flow, and serum immunoreactive secretin levels was studied in dogs. Bile alone had no effect on gastric secretion, but the mixture of bile and olive oil induced prompt, statistically significant gastric secretory inhibition. Bile had the early choleretic effect that would be expected to result from the absorption of bile salts, whereas the bile--olive oil mixture brought about a delayed amd much greater increase in bile flow rates. None of the agents given intraduodenally produced a significant change in the serum secretin level. Intravenous pentagastrin infusion caused a significant increase in rate of bile flow.

Animals↗
PubMed1976

Effect of nicotine on serum secretin and exocrine pancreatic secretion.

The effect of nicotine (100 mug/kg hr-1) on serum secretin and pancreatic secretions was studied in dogs with chronic pancreatic fistulas. Release of immunoreactive secretin (IRS) was stimulated by intraduodenal infusion of HCl (9.6 mEq/30 min). Pancreatic flow rate and bicarbonate and protein secretions were stimulated either by intestinal acidification or infusion of exogenous secretin (1.0 IU/kg hr-1). It was found that nicotine delayed the appearance of peak IRS concentrations in response to intraduodenal HCl by about 20 min. However, nicotine had no effect on the total amount of IRS released nor was this delay accompanied by a similar delay in the appearance of peak bicarbonate output. Furthermore, nicotine did not affect pancreatic secretory function stimulated by either HCl or exogenous secretin. These data do not support the thesis that nicotine plays an important role in the pathogenesis of duodenal ulcers in smokers by inhibiting the pancreatic secretion of bicarbonate.

Animals↗