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Biomedical subjects

G F Cahill

Publications and source records attributed to G F Cahill.

At least 55 records · Page 3Linked to original sources
PubMed1976

Amino acid levels across normal forearm muscle and splanchnic bed after a protein meal.

To characterize further the role of blood cells in amino acid transport, four normal volunteers were asked to ingest 200 g of broiled ground sirloin within a 10-min period. Blood samples from a radial artery, a deep vein draining forearm muscle bed, and a tributary of the hepatic vein were obtained prior to and for 4 hr after the meal and analyzed for various hormones and substrates. At rest, analysis of arterio-deep venous differences across the forearm revealed the blood cell and plasma amino acid compartmentmental contents to be relatively constant except for alanine and glutamine. Whole blood arterio-hepatic venous (A-HV) amino acid differences were not significantly different from zero; however, blood cell A-HV difference analysis revealed a significant release of threonine from the splanchnic bed while plasma A-HV difference analysis revealed modest but significant releases of glutamate and ornithine and uptakes of phenylalanine and histidine. After the ingestion of the meat meal, plasma and blood cell levels of almost all of the measured amino acids increased significantly. Notable exceptions included glycine and alanine, levels of which did not change significantly and glutamine. The arterial blood cell content of the latter amino acid paradoxically decreased while arterial plasma levels increased significantly. Most importantly, large quantities of branched chain amino acids were released from the splanchnic bed and removed by forearm muscle. These data suggest that the blood cells of normal man do actively participate in amino acid transport, and that the magnitude and direction of change induced by the ingestion of a proteins meal varies with the individual amino acid.

Abdomen↗
PubMed1976

Hormone-fuel concentrations in anephric subjects. Effect of hemodialysis (with special reference to amino acids).

Arterial blood concentrations of insulin, glucagon, and various substrates were determined in six anephric subjects in the postabsorptive state and immediately after hemodialysis. Plasma glucose and serum insulin concentrations were normal, and declined during dialysis. Plasma glucagon was elevated and remained unchanged. There was moderate hypertriglyceridemia before dialysis, but this decreased significantly after administration of heparin just before the start of dialysis, and at the end of dialysis was lowered further into the normal range. Comparison of postabsorptive whole blood concentrations of amino acids with those in normal, healthy adults revealed striking differences. Glutamine, proline, citrulline, glycine and both 1- and 3-methyl-histidines were increased, while serine, glutamate, tyrosine, lysine, and branched-chain amino acids were decreased. The glycine/serine ratio was elevated to 300% and tyrosine/phenylalanine ratio was lowered to 60% of normal. To investigate the potential role of blood cells in amino acid transport, the distribution of individual amino acids in plasma and blood cell compartments was studied. Despite a markedly diminished blood cell mass (mean hematocrit, 20.6 +/- 1.4%), there was no significant decrease in the fraction of most amino acids present in the cell compartment, and this was explained by increases of several amino acids in cellular water. None were decreased. Furthermore, during dialysis, whole blood and plasma amino acids declined by approximately 30% and 40%, respectively, whereas no significant change was observed in the cell compartment. Alanine was the only amino acid whose concentration declined in the cells as well as in plasma. The results indicate (a) significant alterations in the concentrations of hormones and substrates in patients on chronic, intermittent hemodialysis; (b) removal of amino acids during hemodialysis, predominantly from the plasma compartment, with no significant change in cell content; and (c) a redistribution of amino acids in plasma and blood cell compartments with increased gradients of most of the amino acids per unit cell water, by mechanism(s) as yet undetermined.

Adult↗
PubMed1975

Anomeric specificty of 3-0-methyl-D-glycopyranose against alloxan diabetes.

The individual alpha and beta anomers of the nonmetabolized glucose analog 3-O-methyl-D-glucopyranose (3MG) were studied as protective agents against the alloxan toxicity to pancreatic beta cells in an in vivo rat model. The alpha 3MG provides greater protection than either the beta or the equilibrated compound, as indicated by plasma glucose concentrations 24 hours after the experiment. This specificity suggests that the beta cell membrane is extremely stereospecific, and that glucose or 3MG provide protection against alloxan injury directly by an interaction with the cell membrane and not by subsequent metabolism of the protecting compound.

Animals↗
PubMed1975

Alanine-induced amino acid interrelationships.

Six normal subjects received 10 g of alanine both orally and as a 60-min intravenous infusion. In both studies blood samples for hormones and substrates were obtained every thirty minutes for 2 1/2 hour. Significant increases in whole blood levels of threonine, serine, glutamine, proline, glycine, and alpha-amino-n-butyric acid were found, which were mainly due to increases of these amino acids in the plasma compartment. In contrast, whole blood levels of leucine, valine, and isoleucine declined, mainly due to increases in the cell compartment. Plasma glucagon levels increased in both studies while insulin levels rose significantly only during the oral study. Plasma free fatty acids and blood glycerol levels declined while lactate and pyruvate increased. Glucose concentration did not change during both tests. These data suggest that the administration of large quantities of alanine is capable of inducing significant alterations in levels of other amino acids and substrates as well as changing hormone levels.

Adult↗
PubMed1975

Metabolic effects of glucose in brief and prolonged fasted man.

The protein-sparing capability of glucose was investigated in overweight subjects prior to and during the performance of prolonged therapeutic fasts. Blood (for hormones and substrates) and urine (for nitrogen and ketoacids) specimens were collected prior to, during, and subsequent to the performance of the following studies. Three subjects ingested, as their only source of calories, 37.5 g of glucose every 6 hours for 7 days (glucose I). The same group of subjects was then fasted for 3 weeks following which the above glucose protocol was repeated (glucose II). In both groups, glucose administration diminished nitrogen excretion, urea being decreased in the first group and ammonia in the second.

Acetoacetates↗
PubMed1975

Effect of alanine and glycine on glucagon secretion in postabsorptive and fasting obese man.

Changes in blood levels of glucagon, insulin and glucose in response to infusions of alanine and glycine have been studied in postabsorptive and fasting obese human subjects. Four-to-five-fold elevations of baseline plasma alanine levels stimulated glucagon secretion significantly. Supraphysiological plasma levels of glycine had a small but insignificant stimulatory effect on glucagon secretion. The glucose increase (6 to 10 mg per 100 ml) observed within 30 min of a supraphysiologic alanine infusion in subjects fasted for 2 or more weeks may be secondary to glucagonmediated glycogen breakdown. However, despite equivalent glucagon rises in the other two study periods, no significant rise in blood sugar was noted during the period of infusion.

Adolescent↗
PubMed1975

Plasma and cerebrosponal fluid amino acid levels in diabetic ketoacidosis before and after corrective therapy.

To evaluate the effect of insulin-saline-bicarbonate therapy on amino acid metabolism in diabetic ketoacidosis, arterial and venous blood samples as well as cerebrospinal fluid (CSF) were obtained from six patients before and after initiation of corrective therapy. Levels of CSF glutamine were decreased while alanine alpha-amino-n-butyrate, valine, isoleucine and leucine were increased significantly compared to a control group composed of six normal, postabsorptive adults free of any neurologic disease. Following therapy, CSF levels of alanine, alpha-amino-n-butyrate, valine, isoleucine, and leucine declined while glutamine levels did not change. Admission arterial plasma levels of the glycogenic amino acids were lower than normal while the branched-chain amino acids were elevated. Plasma alanine and glutamine arterio-venous (A-V) differences across forearm tissue were larger. After four hours of corrective therapy, arterial plasma levels of most of the amino acids had declined sharply and A-V differences for glutamine and alanine were markedly reduced (p smaller than.025 and p smaller than.01, paired t, respectively). Coincident with the decrease in A-V amino acid differences, plasma glucagon and free fatty acid levels declined significantly. These data suggest that the effect exerted by insulin-saline-bicarbonate therapy on amino acid metabolism is manifested by diminished A-V plasma alanine and glutamine differences across forearm tissue. Thus, the role played by the splanchnic bed both before and following corrective measures may be secondary to substrate availability.

Abdomen↗
PubMed1975

Studies of alloxan toxicity on the beta cell.

The ability of sugars to protect the beta cell from alloxan diabetes is highly stereospecific. The alpha anomer, which is present in equilibrium in both glucose and 3-O-methyl glucose (3-OMG) at approximately 34 per cent, provides greater protection than the beta anomer. The greater protection of the alpha anomer of glucose is present fifteen seconds between its administration and alloxan, but there is no difference in protection following a thirty-second interval. The nonmetabolized analogue, 3-OMG, provides even greater protection than glucose, and this higher affinity is expressed both by the lower dose necessary to provide protection, as well as by the higher dose of mannoheptulose needed to remove thr protection. Mannoheptulose not only removes the protection provided by exogenous glucose but sensitizes the beta cell to the toxic effects of alloxan in the fasting state, probably by inhibiting the protection provided by endogenous glucose. Mannoheptulose is able to remove glucose protection before, with, or after the administration of glucose prior to alloxan injection. Finally, the protective effect of both glucose and 3-OMG is time-related, and the protection not only is due to absolute concentration but also appears to be affected by a changing concentration.

Alloxan↗
PubMed1974

Beta cell protection to alloxan necrosis by anomers of D-glucose.

Various concentrations of either the alpha or beta anomers of D-glucose were injected into fasted rats prior to a diabetogenic dose of alloxan. Plasma concentrations of glucose were measured 24 hours later. There was a significantly greater protection of the pancreatic beta cells by the alpha anomer of D-glucose as compared to the beta anomer, which was evidenced by concentrations of glucose in the plasma, and morphology of beta cells.

Alloxan↗