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Biomedical subjects

R A Chez

Publications and source records attributed to R A Chez.

At least 145 records · Page 8Linked to original sources
PubMed1970

Factors affecting the response to insulin in the normal subhuman pregnant primate.

The concentrations of plasma glucose, free fatty acids, insulin, growth hormone, and placental prolactin in subhuman primate fetal and maternal plasma were examined following intravascular administration of insulin and glucagon to the fetus and mother. The neonatal plasma responses to these same stimuli were also examined. Fetal plasma glucose concentrations were minimally altered by direct fetal insulin injections, whereas neonatal glucose levels declined with similar injections. In both instances, however, plasma free fatty acid levels declined following insulin. When the amount of insulin given the fetus was increased, fetal plasma glucose concentrations did decline. Combined intravascular insulin injections and infusions in the mother were associated with a disappearance of the initial maternal to fetal plasma glucose concentration gradient and a nearly parallel fall in both maternal and fetal plasma glucose levels. It was concluded that insulin was biologically active in the fetus. Obtunded fetal plasma glucose responses to direct fetal insulin administration may be a function of placental transfer of glucose from the maternal pool. Maternal plasma placental prolactin and fetal plasma growth hormone levels were unchanged in the presence of sustained maternal and fetal hypoglycemia. However, neonatal plasma growht hormone levels did increase in response to hypoglycemia. The observed bidirectional placental barrier to transfer of radioisotopically labeled growth hormone indicated that fetal plasma growth hormone was solely of fetal origin. These data suggested further that a change in the growth hormone-releasing mechanism may occur from fetal to neonatal life. Direct maternal intravascular glucagon administration led to augmentation in both maternal and fetal plasma insulin and glucose levels. Direct fetal glucagon injections enhanced both maternal and fetal plasma insulin levels. These simultaneous changes in both plasma pools were consistent with the demonstration of a bidirectional placental transfer of radioisotopically labeled glucagon. The role of endogenously produced glucagon in these studies remains to be clarified.

Animals↗
PubMed1969

Fetal insulin and growth hormone metabolism in the subhuman primate.

The concentrations of plasma glucose, insulin, growth hormone, and immunoreactive growth hormone-like substance in subhuman primate fetal and maternal plasma were examined after the intravascular administration of glucose, arginine, or tolbutamide to the fetus. Cannulation of interplacental vessels permitted studies on the fetus in utero without disruption of fetal-placental-maternal anatomic integrity. Single glucose injections, glucose infusions, and arginine infusions into the fetus did not alter fetal plasma insulin concentrations. In contrast, tolbutamide injections elicited an immediate 3-4-fold increase in fetal plasma insulin concentrations. A bidirectional placental transfer of insulin was demonstrated with the use of simultaneously injected insulin-(125)I to the mother and insulin-(131)I to the fetus. Simian fetal plasma contained a substance which cross-reacted with immunologic identity to human growth hormone. In contrast, simian maternal plasma and amniotic fluid reacted with immunologic nonidentity to human growth hormone. Although glucose administration to the fetus did not suppress nor did arginine infusion consistently augment fetal plasma growth hormone levels, the latter were observed to vary in individual experiments. The plasma responses to the same stimuli in the neonate were also examined. In contrast to the fetal experiments, glucose injection in the neonate elicited a delayed rise in the concentration of plasma insulin. Similar to the fetus, the plasma concentration of insulin increased after tolbutamide injection and did not change in response to arginine infusion. The initial concentrations of neonatal plasma growth hormone were significantly lower when contrasted with the initial fetal plasma levels. There was no difference in the responsiveness of the fetal and neonatal growth hormone-releasing mechanisms when challenged by glucose or arginine infusion. The data indicate that the fetal plasma concentration of growth hormone is labile, that fetal growth hormone metabolism may differ from that in the neonate, and that pancreatic islet cell responsiveness rapidly changes after delivery.

Animals↗
PubMed1967

Effect of inhibitors on alanine transport in isolated rabbit ileum.

The effects of metabolic inhibitors and ouabain on alanine transport across rabbit ileum, in vitro, have been investigated. Net transport of alanine and Na across short-circuited segments of ileum is virtually abolished by cyanide, 2,4-dinitrophenol, iodoacetate, and ouabain. However, these inhibitors do not markedly depress alanine influx from the mucosal solution, across the brush border, into the intestinal epithelium, and they do not significantly affect the Na dependence of this entry process. The results of this investigation indicate that: (a) the Na dependence of alanine influx does not reflect a mechanism in which the sole function of Na is to link metabolic energy directly to the influx process; and (b) the inhibition of net alanine transport across intestine is, in part, the result of an increased rate coefficient for alanine efflux out of the cell across the brush border. Although these findings do not exclude a direct link between metabolic energy and alanine efflux, the increased efflux may be the result of the increased intracellular Na concentration in the presence of these inhibitors. The results of these studies are qualitatively consistent with a model for alanine transport across the brush border which does not include a direct link to metabolic energy.

Alanine↗
PubMed1967

Alanine and sodium fluxes across mucosal border of rabbit ileum.

Unidirectional influxes of L-alanine and Na from the mucosal solution into the epithelium of in vitro rabbit ileum have been determined. In the presence of 140 mM Na, alanine influx is approximately 2.2 micromoles/hr cm(2), but is inhibited if the NaCl in the mucosal solution is replaced by choline Cl, Tris-Cl, mannitol, LiCl, or KCl. Although alanine influx is strongly dependent upon Na in the mucosal solution, it is uninfluenced by marked reduction of intracellular Na pools. In addition, alanine influx is unaffected by intracellular alanine concentration. Na influx is markedly inhibited by the presence of Li. Evidence is presented that Na transport across the mucosal border cannot be attributed to simple diffusion even though the net flux across this surface is in the direction of the electrochemical potential difference.

Alanine↗
PubMed1967

Kinetic relations of the Na-amino acid interaction at the mucosal border of intestine.

The relation between unidirectional influxes of Na and amino acids across the mucosal border of rabbit ileum was studied under a variety of conditions. At constant Na concentration in the mucosal bathing solution, amino acid influx followed Michaelis-Menten kinetics permitting determination of maximal influx and the apparent Michaelis constant, K(t). Reduction in Na concentration, using choline as substitute cation, caused an increase in K(t) for alanine but had no effect on maximal alanine influx. The reciprocal of K(t) was a linear function of Na concentration. Similar results were obtained for valine and leucine and these amino acids competitively inhibited alanine influx both in the presence and in the absence of Na. These results lead to a model for the transport system which involves combination of Na and amino acid with a single carrier or site leading to penetration of both solutes. The model predicts that alanine should cause an increase in Na influx and the ratio of this extra Na flux to alanine flux should vary with Na concentration. The observed relation agreed closely with predicted values for Na concentrations from 5 to 140 mM. These results support the hypothesis that interactions between Na and amino acid transport depend in part on a common entry mechanism at the mucosal border of the intestine.

Alanine↗
PubMed1966

Effect of sugars on transport of alanine in intestine.

The eflect of glucose and galactose on transport of alanine by rabbit ileum has been investigated. Transmural transport and cellular ac cumulation of the amino acid were in hibited by the sugars, but alanine in flux across the mucosal border of the cells was unaltered.

Alanine↗