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Biomedical subjects

J Dupre

Publications and source records attributed to J Dupre.

At least 73 records · Page 4Linked to original sources
PubMed1978

Initial splanchnic extraction of ingested glucose in normal man.

Estimates of initial splanchnic uptake of ingested glucose and the concomitant suppression of endogenous glucose production were obtained in man by validated tracer techniques for non--steady-state turnover measurement. Nine normal volunteers (18--44 yr old) fasted overnight received intravenous infusions of tracer (3-3H-glucose or 1-14C-glucose) and a low (45 +/- 1 g) or high (96 +/- 5 g) oral load of glucose labeled with an alternative tracer (1-14C-glucose or 2-2H-glucose). A two-compartment model was used to derive rates of peripheral appearance (Ra) of glucose from all sources (total) and the Ra of ingested glucose. Ra (total glucose) and Ra (ingested glucose) were integrated from the first appearance of ingested glucose until the basal Ra (total glucose) or 116 +/- 6 (SEM) mg/min was reattained. The total amount of glucose reaching the systemic pool in this time was 95 +/- 4 g and 46 +/- 3 g with high and low doses, respectively. Of these quantities 86 +/- 4 g and 40 +/- 3 g originated in the oral glucose, representing 90% +/- 4% of the administered glucose. The remainder (11% +/- 2% of the total) represented endogenous production, suppressed by 66% +/- 6% relative to basal. Sequestration of ingested glucose and subsequent release did not take place during the study since identical results were obtained with ingested 1-14C-glucose or 2-3H-glucose. The latter label would have been lost if the glucose had entered the hexose--phosphate pool. Thus, in normal man approximately 90% of an ingested glucose load is absorbed and passes through the liver to appear in the systemic pool.

Absorption↗
PubMed1978

Glucose tolerance during anaesthesia and surgery. Comparison of general and extradural anaesthesia.

The effects of general and extradural anaesthesia on glucose tolerance and plasma cortisol concentration in the surgical patient were assessed. Normal glucose tolerance and insulin release were observed under extradural anaesthesia, whereas general anaesthesia produced decreases in both glucose tolerance and insulin release. The plasma cortisol concentration was increased in both groups. These results indicate possible nutritional advantages in conducting surgery under extradural anaesthesia.

Adult↗
PubMed1978

Effects of ingestion of triglyceride or galactose on secretion of gastric inhibitory polypeptide and on responses to intravenous glucose in normal and diabetic subjects.

Responses of plasma immunoreactive gastric inhibitory polypeptide (IRGIP) to oral triglyceride or galactose were compared in normal and mildly diabetic (non-insulin-dependent) subjects. After triglyceride the responses of IRGIP were similar, but after galactose those of the diabetics were slightly exaggerated. Both stimuli evoked increments of plasma immunoreactive glucagon (IRG) in diabetics but not in normal subjects. Plasma immunoreactive insulin (IRI) did not change. In normal subjects given oral triglyceride or galactose followed by intravenous (I.V.) glucose the early-phase response of plasma IRI was enhanced and glucose tolerance improved. In the diabetics, oral triglyceride did not affect insulin release or glucose tolerance after I.V. glucose; oral galactose elicited a slight increase of insulin release without improving glucose tolerance. In the diabetics the rise of plasma IRG after ingestion of triglyceride or galactose was maintained after I.V. glucose. It is concluded that endogenous GIP is insulinotropic and that there is partial resistance to this action in diabetes. The results were compatible with feedback inhibition of GIP secretion by insulin and with the suggestion that the rise of plasma IRG associated with secretion of GIP in diabetics may be due to the glucagonotropic action of this peptide.

Administration, Oral↗
PubMed1976

Inhibition of actions of glucagon in adipocytes by gastric inhibitory polypeptide.

Possible interactions between gastric inhibitory polypeptide (GIP) and glucagon were investigated in rat adipocytes. GIP was nonlipolytic and inhibited lipolysis stimulated by glucagon but not that stimulated by secretin or vasoactive intestinal polypeptide (VIP). GIP competed with 125I-glucagon for binding to adipocyte receptors, and at physiologic concentrations inhibited the stimulation of AMP produced by glucagon. Thus GIP acts as an inhibitor of actions of glucagon on adipocytes and may be a physiologic modulator of effects of glucagon.

Adipose Tissue↗
PubMed1976

Effects of brief starvation on muscle amino acid metabolism in nonobese man.

A reduction in the release of substrate amino acids from skeletal muscle largely explains the decrease in gluconeogenesis characterizing prolonged starvation. Brief starvation is associated with an increase in gluconeogenesis, suggesting increased release of amino acids from muscle. In the present studies, accelerated amino acid release from skeletal muscle induced by brief starvation was sought to account for the accompanying augmentation of gluconeogenesis. To do this amino acid balance across forearm muscles was quantified in 15 postabsorptive (overnight fasted) subjects and in 7 subjects fasted for 60 h. Fasting significantly reduced basal insulin (11.3-7.5 muU/ml) and increased glucagon (116-134 pg/ml). Muscle release of the principal glycogenic amino acids increased. Alanine release increased 59.4%. The increase in release for all amino acids averaged 69.4% and was statistically significant for threonine, serine, glycine, alanine, alpha-aminobutyrate, methionine, tyrosine, and lysine. Thus, with brief starvation, muscle release of glycogenic amino acids increases strikingly. This contrasts with the reduction of amino acid release characterizing prolonged starvation. The adaptation of peripheral tissue metabolism to brief starvation is best explained by the decrease in insulin.

Adult↗
PubMed1976

Metabolism of forearm tissues in man. Studies with glucagon.

The role of glucagon in regulating peripheral tissue metabolism in man was assessed in the present studies. To do this, glucagon was infused for two hours into the brachial artery to produce a high but physiologic increment in the glucagon content of arterial blood supplying ipsilateral tissues. Metabolic effects on muscle and on subcutaneous adipose tissue plus skin were sought in seven overnight-fasting subjects and seven subjects starved briefly (60 hours). In the overnight-fasted group the infusion increased bassl glucagon concentration by 1,216 pg./ml. but was without effect on forearm tissue metabolism of glucose, lactate,glycerol, or amino acids. Starvation significantly reduced basal insulin (11.0 to 7.4 muU./ml.) and increased endogenous glucagon (116 to 134 pg./ml.). Basally, there was substantial ketone utilization and a decrease in glucose consumption by both muscle and subcutaneous adipose tissue plus skin. The glucagon infusion increased basal glucagon by 784 pg./ml. Muscle balances of glucose, lactate, acetoacetate, amino acids, and glycerol were unaffected. The metabolism of glucose, lactate, acetoacetate, glycerol, and free fatty acids by subcutaneous adipose tissue plus skin was also unchanged. It is concluded that physiologic increments of glucagon lasting two hours are without effect on forearm tissues in overnight-fasted and briefly starved man.

Acetoacetates↗
PubMed1975

Interaction of secretin and insulin on human forearm metabolism.

The effect of secretin on forearm metabolism (muscle compartment) was examined in the presence of low and high concentrations of insulin. Continuous infusions (30 min. duration) of secretin 12 ng/min. (SEC), insulin 160 ng/min. (INS) or these doses of insulin and secretin together (INS + SEC) were delivered into the brachial arteries of normal volunteers. SEC alone was without significant effect on forearm metabolism. INS as previously reported, stimulated glucose and potassium uptake and inhibited the output of some amino acids from the deep venous bed. The two hormones together (INS + SEC) increased maximum lactate (p less than 0.025) and alanine output (p less than 0.005) beyond that observed with INS alone. A marked calcium output occurred (p less than 0.001) with the combined infusion which was not observed with either hormone alone. Potassium metabolism with INS + SEC was similar to that observed with INS alone. These results suggest that these two hormones, acting in concert, stimulate glycolysis and net calcium efflux. This joint action of insulin and secretin may have a physiological role in the immediate postprandial period.

Adult↗
PubMed1975

Effects of portacaval anastomosis on glucose tolerance in the dog: evidence of an interaction between the gut and the liver in oral glucose dosposal.

Continuous infusions of glucose (90 min duration) were given into the duodenum (ID), or the portal vein (IP), or a peripheral vein (IV) in conscious dogs, intact dogs, or dogs with portacaval anastomoses. In intact animals ID glucose tolerance was better than IV glucose tolerance, but IP glucose tolerance was not significantly different from IV glucose tolerance. Thus, the superiority of tolerance to ID glucose was not accounted for by relatively high levels of glucose in portal blood. IV glucose tolerance was not significantly affected by protacaval anastomosis with ligation of the portal vein, but ID glucose tolerance was markedly impaired. Disproportionate impairment in tolerance to enterically administered glucose in dogs with portacaval shunts, and the similarity of IP and IV glucose tolerance in intact dogs, suggest that both liver and the gut are important in determination of oral glucose tolerance through mechanisms that have little or no effect on responses to parenterally administered glucose. The results also suggest that the hepatic contribution is not dependent upon portal venous perfusion of the liver, and that a humoral interaction between the gut and the liver is involved which is not simply dependent on endocrine responses of the pancreas.

Animals↗
PubMed1969

Effects of secretin, pancreozymin, or gastrin on the response of the endocrine pancreas to administration of glucose or arginine in man.

Intravenous administration of porcine secretin or pancreozymin or synthetic human gastrin II resulted in raised increments in serum immunoreactive insulin during intravenous infusion of glucose in normal man. Enhancement of serum immunoreactive insulin by each hormone was associated with accelerated disposal of glucose. In response to prolonged intravenous infusion of arginine with pancreozymin there was a maintained rise in immunoreactive insulin and glucagon-like immunoreactivity in the blood. These effects of pancreozymin and arginine were not reproduced with secretin and arginine, and may have been due to the stimulation of glucagon secretion together with insulin by pancreozymin. Enteric infusion of hydrochloric acid, or stimulation of gastric acid secretion by betazole, presumed to cause release of endogenous secretin, led to enhancement of insulin secretion during intravenous infusion of glucose. Enteric infusion of arginine, presumed to cause release of endogenous pancreozymin, led to a rise in serum immunoreactive insulin not attributable to effects of circulating glucose and amino acids. It is concluded that secretin and pancreozymin released in response to physiological stimuli contribute to stimulation of the endocrine pancreas after ingestion of food.

Adolescent↗
PubMedDate not supplied

Continuous subcutaneous insulin infusion in adults: glycemic advantage is predicted by venous plasma C-peptide concentrations.

Continuous subcutaneous insulin infusion (CSII) has been compared with conventional insulin injection treatment (CIT) supplemented by self-monitoring of capillary blood glucose (SMBG) in 18 nonobese adults with insulin-dependent diabetes mellitus (IDDM). Mean daily insulin dosage and rates of hypoglycemia were similar during CSII (duration of treatment 36 +/- 2 wk mean +/- SE) and CIT (31 +/- 1.6 wk). On the basis of fasting C-peptide concentrations and postintravenous glucagon increments of less than 0.1 pmol/ml, subjects were classified C-peptide negative (CP NEG) (N = 11), or C-peptide positive (CP POS) (N = 7). Relative to CIT, CP NEG subjects on CSII had significant decreases in premeal/bedtime and postmeal plasma glucose concentrations and glycosylated hemoglobin (percent of total). CP POS patients during each of CSII and CIT showed glycemic responses equivalent to those of CP NEG patients on CSII. In neither group could results be explained on the basis of improved beta cell function. Thus, therapeutic advantage of CSII was not apparent in IDDM adults retaining significant C-peptide activity.

Adult↗