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Biomedical subjects

L Orci

Publications and source records attributed to L Orci.

At least 487 records · Page 27Linked to original sources
PubMed1973

Exocytosis-endocytosis coupling in the pancreatic beta cell.

The stimulation of the release of insulin by glucose is accompanied by an enhanced uptake of cytochemically demonstrable horseradish peroxidase into endocytotic vesicles within the beta cells. An exocytosis-endocytosis coupling might represent a mechanism by which membrane constituents are recycled within the beta cells under conditions of increased secretory activity.

Animals↗
PubMed1973

Pronase effect on pancreatic beta cell secretion and morphology.

Pronase at low concentration (4 micrograms per milliliter) produces a reversible increase of glucose-stimulated insulin release in isolated islets of Langerhans. Pronase also affects the ultrastructure of the beta cells by inducing extensive development of tight junctions as well as the accumulation of secretory product within the extracellular spaces.

Animals↗
PubMed1973

Insulin release by emiocytosis: demonstration with freeze-etching technique.

The technique of freeze-etching for electron microscopy applied to isolated islets of Langerhans has permitted a successful evaluation of emiocytotic events on the cell surface. The frequency of these events in stimulated cells suggests that emiocytosis represents a significant mechanism for insulin release.

Animals↗
PubMed1973

Dynamics of insulin release and microtubular-microfilamentous system. I. Effect of cytochalasin B.

In order to assess the participation of the microfilamentous cell web in the multiphasic response of the pancreatic beta cell, the effect of cytochalasin B upon both glucose- and sulfonylurea-induced insulin release was investigated in the perfused isolated pancreas. Cytochalasin B failed to affect the basal rate of insulin release, but enhanced the initial and later phases of insulin secretion in response to either glucose or gliclazide. In addition, cytochalasin B lowered the threshold concentration for the stimulant action of glucose upon insulin release. Ultrastructural studies supported the concept of a specific interaction of cytochalasin B with the microfilamentous cell web of the beta cell. It is concluded that the integrity of such a structure is equally important for both the initial and later secretory responses of the beta cell to various insulinotropic agents.

Animals↗
PubMed1973

Glucagon release induced by pancreatic nerve stimulation in the dog.

A direct neural role in the regulation of immunoreactive glucagon (IRG) secretion has been investigated during stimulation of mixed autonomic nerves to the pancreas in anesthetized dogs. The responses were evaluated by measurement of blood flow and hormone concentration in the venous effluent from the stimulated region of pancreas. Electrical stimulation of the distal end of the discrete bundles of nerve fibers isolated along the superior pancreaticoduodenal artery was invariably followed by an increase in IRG output. With 10-min periods of nerve stimulation, the integrated response showed that the higher the control glucagon output, the greater was the increment. Atropinization did not influence the response to stimulation. That the preparation behaved in physiologic fashion was confirmed by a fall in IRG output, and a rise in immunoreactive insulin (IRI) output, during hyperglycemia induced by intravenous glucose (0.1 g/kg). The kinetics of this glucose effect on IRG showed characteristics opposite to those of nerve stimulation: the lower the control output, the less the decrement. Furthermore, during the control steady state, blood glucose concentration was tightly correlated with the IRI/IRG molar output ratio, the function relating the two parameters being markedly nonlinear. Injection or primed infusion of glucose diminished the IRG response to simultaneous nerve stimulation. Measurement of IRG was inferred to reflect response of pancreatic glucagon secretion on the basis of the site of sample collection (the superior pancreaticoduodenal vein), the absence of changes in arterial IRG, and similar responses being obtained using an antibody specific for pancreatic glucagon. THESE STUDIES SUPPORT A ROLE FOR THE AUTONOMIC NERVOUS SYSTEM IN THE CONTROL OF GLUCAGON SECRETION: direct nerve stimulation induces glucagon release. Such sympathetic activation may be interpreted as capable of shifting the sensitivity of the A cell to glucose in the direction of higher glycemia for a given glucagon output. The experimental model employed is valid for further studies of regulatory mechanisms of endocrine pancreatic function in vivo.

Animals↗