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Biomedical subjects

P M Daniel

Publications and source records attributed to P M Daniel.

At least 73 records · Page 4Linked to original sources
PubMed1975

The requirements of the brain for some amino acids.

1. A constant specific activity of radioactively labelled amino acids was maintained in the circulation by means of a new technique devised for this purpose. This has made it possible to measure accurately the entry rates of amino acids into the brain in vivo. 2. The rates of entry into the brain of seven nutritionally non-essential amino acids were measured. 3. Glycine and proline enter the brain relatively slowly, at rates comparable to those of amino acids which are not normally found in the blood. Thus their entry is due mainly if not entirely to passive diffusion. 4. Serine (which is used by the brain to make glycine) and alanine (which is used to make glutamate and aspartate) enter the brain as rapidly as the essential amino acids and thus, although not essential for the body as a whole, appear to be essential for the brain. 5. It is suggested that those amino acids that the brain is able to synthesize have low rates of entry, even though they are present at high concentrations in the plasma, but that the transport systems for those amino acids that are not synthesized in the brain ensure rapid entry at rates that are related to the rates of cerebral utilization.

Alanine↗
PubMed1975

Insulin-stimulated entry of glucose into muscle in vivo as a major factor in the regulation of blood glucose.

1. The entry of glucose into the pectoralis major muscle of living rats was measured over a wide range of plasma glucose concentrations. A technique was used by which steady concentrations of substances are maintained in the circulation throughout the experiments. 2. Raising the concentration of glucose in the plasma caused saturation of the mechanism by which it is transported into muscle. Estimates of the values of the kinetic constants for this transport system were: Kt, 34 mumole ml-1 and V, 1-2 mumole min-1-g-1 muscle. 3. When the plasma glucose concentration was raised up to at least twelve times normal, there was no sign of saturation of the transport system in insulin-treated animals. This finding could be explained if insulin increased greatly both V and Kt for glucose transport. 4. Insulin increased the rate of entry of glucose into muscle over the entire range of plasma glucose concentrations studied (4-8 mumole ml.-1). There was evidence that endogenous insulin produced a similar increase in entry rate some 10 min after the injection of glucose. Fasting, which is associated with a decrease in insulin level, depressed the rate of entry. In hyperglycaemia insulin caused a rise in the concentration of glucose within the muscle cells. 5. The insulin-induced increase in the rate of glucose entry into muscle ensured that approximately 25% of an I.V. dose of glucose entered the muscle cells of insulin-treated animals within one minute. This illustrates the quantitatively important regulatory role that skeletal muscle plays in these circumstances in limiting the extent of a rise in circulating glucose.

Animals↗
PubMed1975

The effect of atropine on insulin release caused by intravenous glucose in the rhesus monkey.

Glucose was given as a rapid intravenous injection to fasted anaesthetized rhesus monkeys, and the concentrations of blood glucose and plasma insulin were measured. Glucose caused a biphasic insulin response. The first phase (which was short) occurred 1 min after the injection; the second was longer, and occurred 17 to 30 min after the injection. Following the control glucose injection, each animal was given atropine, and the insulin response to an identical glucose stimulus was measured. This produced a mean reduction of 45% in the area under the curve of insulin release. Both phases of insulin release were inhibited by atropine. When glucose was given alone, its mean half-time of disappearance from the circulation (t1/2) was 25.4 ( plus or minus 1.9 SEM) min. After atropine the mean t1/2 was 36.6 (plus or minus 3.1 SEM) min, a significant difference. It is suggested that the delayed rate of disappearance of glucose from the circulation is the result of inhibition of insulin release by atropine.

Animals↗
PubMed1974

Saturation of a shared mechanism which transports L-arginine and L-lysine into the brain of the living rat.

1. The rate of entry of L-arginine and L-lysine into the brain of the rat was measured in vivo by a direct method in which the amino acid concentration was at a constant level in the blood plasma over the period of the experiment.2. Both L-arginine and L-lysine enter the brain by a transport mechanism which can be saturated by a high concentration of the same amino acid in the bloodstream. The rate of entry can be explained by Michaelis-Menten kinetics.3. The entry into the brain of L-arginine can be inhibited by raised plasma concentrations of L-lysine or L-ornithine and the entry of L-lysine by raised concentrations of L-arginine.4. The inhibition of entry of an amino acid is most severe when its own concentration in the blood plasma is low and that of the inhibitor is high. The inhibition appears to be basically competitive in type, suggesting that common transport systems are shared by three dibasic amino acids.5. It is suggested that the raised levels of amino acids found in various disorders of amino acid metabolism are likely to reduce the rate of entry into the brain of other amino acids and a way is suggested in which the dietary treatment of hyperlysinaemia may be made more effective.

Animals↗