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Biomedical subjects

J M Conlon

Publications and source records attributed to J M Conlon.

At least 325 records · Page 18Linked to original sources
PubMed1981

Characterization of somatostatin-like components in the tumors and plasma of a patient with a somatostatinoma.

Somatostatin-like immunoreactive polypeptides with approximate molecular weights of 1,500-2,000 (peak I), 2,500-3,500 (peak II), and 10,000-15,000 (peak III) were isolated from the peripheral plasma and from extracts of tumor tissue of a patient with a pancreatic somatostatinoma and hepatic metastases. The peak I component had approximately the same molecular charge as somatostatin, but the peak II component was appreciably more basic. The peak III component was heterogeneous with respect to charge and dissociated into smaller immunoreactive polypeptides during isoelectric focusing or after treatment with strongly denaturing solvents. In plasma, the levels of the larger molecular weight components (peak II and peak III), relative to that of the somatostatin-size component (peak I), were higher than in tissue extracts, suggesting a lower rate of clearance of the larger polypeptides from the circulation. In response to a nutrient stimulus, the peak I component increased to a greater extent than the larger components. Plasma levels of larger immunoreactive polypeptides relative to the peak I component in patient's plasma were higher after complete resection of the pancreatic tumor than preoperatively, suggesting that the rate of release of these putative precursor forms from the metastases was greater than from the primary tumor.

Chemical Phenomena↗
PubMed1979

Somatostatinoma syndrome. Biochemical, morphologic and clinical features.

Diabetes mellitus, steatorrhea, cholelithiasis and a tumor distorting the duodenum prompted a work-up for somatostatinoma in a 52-year-old man. The responses of pancreatic B-cells but not of A-cells to nutrient stimuli were inhibited, and growth-hormone release was suppressed, suggesting somatostatin resistance in some target tissues. Plasma somatostatin-like immunoreactivity ranged from 9000 to 13,000 pg per milliliter (normal: 88+/-8, mean +/- S.E.M.) and was distributed in four molecular forms, including free somatostatin. The primary tumor contained 5 microgram of somatostatin-like immunoreactivity per milligram of wet tissue, distributed in three of the molecular forms noted in plasma. Plasma calcitonin was also elevated (4650 pg per milliliter; normal: less than 120). Immunocytochemical studies showed that cells of the primary tumor contained somatostatin and calcitonin but no other peptide hormones. Only somatostatin was present in the metastases. Somatostatin was localized electron microscopically in all secretory granules, irrespective of size and shape, whereas calcitonin was present only within a single subpopulation of small granules in the same cells.

C-Peptide↗
PubMed1979

Physicochemical and biological properties of glucagon-like polypeptides from porcine colon.

Polypeptide material displaying glucagon-like immunoreactivity was isolated from porcine colon using immunoaffinity chromatography. The immunoreactive material was tightly bound to high molecular weight proteins but was dissociated by 0.1% w/v sodium dodecyl sulphate solution into immunoreactive components of approximate molecular weights 12,000,8000,5000 and 3000. These components reacted at least 50 times more strongly with antibodies specific for the N-terminal region of glucagon than with antibodies specific for the C-terminal region of glucagon. While the 8000 and 3000 dalton fractions were homogeneous, the 12,000 and 5000 dalton fractions were resolved into multiple bands by isoelectric focusing. The 12,000 dalton fraction was devoid of glycogenolytic and lipolytic activity, was not insulin releasing and showed no ability to bind to receptor sites specific for glucagon on hepatic plasma membranes and to active hepatic adenylate cyclase. The 8000 and 5000 dalton components showed weak lipolytic activity. The possible significance of colonic glucagon-like immunoreactivity relative to pancreatic glucagon and immunoreactivity from other tissues is discussed.

Adenylyl Cyclases↗
PubMed1979

The use of perfused rat intestine to characterise the glucagon-like immunoreactivity released into serosal secretions following stimulation by glucose.

Isolated perfused intestine of rat was used to demonstrate the glucose-stimulated release of glucagon-like immunoreactivity (GLI) into serosal secretions. The released GLI was characterised using immunoaffinity chromatography on columns of immobilised antibodies specific for the N (residues 1 to 18) and for the C (residues 19-29) terminal portions of glucagon followed by gel-filtration. The immunoreactivity was present in a variety of molecular species. These include a large GLI which has a molecular weight about 12000 and binds to antibodies specific for the N-terminal portion of glucagon and two polypeptide fractions with molecular weight closer to that of glucagon. While one fraction of the small GLI boun both to antibodies specific for the C-terminal and N-terminal portions of glucagon the other bound only to the former antibodies. The relevance of these findings to the origins of circulating GLI and the possible precursor relationship between large and other forms of GLI is discussed.

Animals↗
PubMed1979

Pancreatic and gastric release of somatostatinlike immunoreactivity during intestinal phase of a meal.

The present study was designed to examine pancreatic and gastric D-cell function during the intestinal phase of a liver meal. The intraduodenal instillation of a 20% liver meal (5 ml/min) elicited a significant rise in the plasma levels of somatostatinlike immunoreactivity (SLI) in the pancreatic vein and inferior vena cava, together with the rise in glucagon and insulin levels. The rise in pancreatic vein SLI was not reduced after truncal vagotomy or during atropine infusion. In the stomach, the intestinal liver meal elicited a significant rise in antral but not fundic vein SLI levels. The rise in antral vein SLI was augmented after truncal vagotomy and abolished during atropine infusion, as was the rise in inferior vena caval SLI. In contrast to the protein meal, intravenous infusion of an amino acid mixture elicited a rise in pancreatic vein SLI but not antral or fundic vein SLI. It is concluded that during the intestinal phase of a protein meal, pancreatic and antral but not fundic SLI release is stimulated. The effects of truncal vagotomy and atropine infusion on these responses suggest a close interaction between the vagus and muscarinic cholinergic mechanisms and the D cells of the stomach and pancreas.

Animals↗
PubMed1979

Properties of somatostatin-like immunoreactive polypeptides in the canine extrahypothalamic brain and stomach.

Polypeptides with somatostatin-like immunoreactivity (SLI) and approximate molecular weights of 12,000, 3,000, and 1,600 were isolated from acid extracts of the canine extrahypothalamic brain and stomach by affinity chromatography, ion exchange, gel filtration, and isoelectric focusing. The 12,000-dalton SLI was acidic, whereas the 3,000- and 1,600-dalton forms were basic molecules. All SLI fractions diluted proportionally in a RIA employing an antibody directed toward the central region of somatostatin. Like synthetic somatostatin, the 1,600-dalton SLI inhibited pentagastrin-stimulated gastric acid secretion in rats. Neither of the two larger forms of SLI were dissociated by 6 M guanidinium HCl. However, treatment with dithiothreitol, which reduces disulfide bonds, resulted in the conversion of a large portion of the 12,000-dalton SLI to the 1,600-dalton form. These data are compatible with a model of a 12,000-dalton SLI consisting of somatostatin bound to an acidic polypeptide by a peptide bond and a disulfide bond. Variations in the relative rates of hydrolysis of the peptide bonds and reduction of the disulfide bonds in different tissues may result in three forms of the 12,000-dalton polypeptide in which both bonds are intact or one of the two bonds is cleaved.

Animals↗
PubMed1979

Glucagon-like polypeptides in canine brain.

Glucagon-like material has been detected by radioimmunoassay in several areas of the canine brain. High concentrations of glucagon-like immunoreactivity (GLI), measured with antibodies directed against the N-terminal region of glucagon, have been found in the hypothalamus, amygdala, and mesencephalon, but a high concentration of immunoreactive glucagon (IRG), measured with antibodies directed against the C-terminal region of glucagon, has been found only in the hypothalamus. The predominant molecular forms of GLI isolated from brain extracts by affinity chromatography are the same as those isolated from gut extracts. The predominant form of IRG in brain extracts is of the same (approximate) molecular weight as pancreatic glucagon.

Animals↗
PubMed1979

Release of somatostatin-like immunoreactivity from the lower gut.

The present study describes the effect of the instillation of a nutrient-containing hyperosmolar volume load into the lower ileum upon plasma levels of somatostatin-like immunoreactivity. The baseline levels of SLI in the mesenteric vein were significantly higher than those in the inferior vena cava and rose significantly in both veins in response to the nutrient load. SLI levels in the venous effluent of the pancreas and stomach did not rise. Mesenteric vein SLI was similar in molecular size to the SLI in the gastric and pancreatic veins and to synthetic somatostatin. The results suggest that the lower gut may contribute to the basal circulating SLI levels and that it is released from the lower gut in response to a nutrient-containing hyperosmolar volume load.

Animals↗
PubMed1978

Pancreatic and gastric somatostatin release in response to intragastric and intraduodenal nutrients and HCl in the dog.

The effects of the instillation of glucose, fat, casein hydrolysate, and HCl into the gastrointestinal tract upon plasma levels of somatostatin-like immunoreactivity (SLI) in the venous effluent of the pancreas, fundus and antrum of the stomach, and in the inferior vena cava (IVC) were determined in normal laparotomized dogs. Fasting SLI levels in the effluent plasma from these sites were significantly greater than IVC levels. The intragastric administration of glucose elicited a prompt and significant rise in SLI levels in pancreatic, fundic and antral venous plasma, and in IVC plasma; intraduodenal glucose elicited smaller increments. After intragastric fat, a smaller, more gradual increase in the pancreatic and fundic effluents was observed, whereas the rise in antral SLI was minute, and IVC SLI did not rise significantly. Intraduodenal fat elicited a prompt increase in the pancreatic and antral vein SLI levels, and a small but significant increase in fundic and IVC plasma which suggests faster release of enteric factors that influence SLI secretion in the pancreas and antrum. Intragastric casein hydrolysate elicited a prompt increase in SLI in both the pancreatic and fundic veins, the latter being marked, but the antral SLI response was small; IVC SLI rose significantly within 15 min. Intragastric HCl provoked a prompt and marked rise in pancreaticoduodenal and antral vein SLI but no increase in fundic vein SLI; IVC SLI levels rose significantly within 20 min. Intraduodenal HCl elicited an even more prompt and marked pancreatic SLI response, and SLI rose significantly in both the fundic and antral venous effluents; IVC SLI also rose more promptly. In dogs with a gastric fistula that prevented intraduodenal entry of HCl, intragastric HCl elicited only a very small and transient rise in pancreaticoduodenal vein SLI, markedly stimulated the antral SLI response, but completely suppressed fundic venous SLI levels. The results indicate that all three nutrients stimulate SLI release from the pancreas and stomach. The greater SLI response to intragastric, as opposed to intraduodenal, glucose suggests that unidentified local factors are of importance. The responses to the intraduodenal instillation of HCl and fat suggest a role of enteric hormones in the release of SLI from the pancreas and fundus and antrum of the stomach. Additionally, there is evidence of direct effects of HCl upon gastric SLI release.

Animals↗
PubMed1978

Properties of endogenous somatostatin-like immunoreactivity and synthetic somatostatin in dog plasma.

Somatostatin-like immunoreactivity (SLI) in the peripheral venous plasma of dogs and in their pancreatic and gastric venous effluents was characterized and compared with synthetic somatostatin. Both endogenuous plasma SLI and somatostatin added to plasma were eluted from Sephadex gels at pH 8.8 in the 150,000--200,000-mol wt region but at pH 2.5 both appeared in the 1,500--2,000-mol wt region. The SLI released from the isolated dog pancreas perfused with plasma-free buffer was eluted entirely as a 1,600-dalton polypeptide, but when the pancreas was perfused with plasma, SLI was eluted in the 150,000--200,000-mol wt zone. Affinity chromatography of plasma samples on immobilized antibodies directed against the central portion of the somatostatin molecule (residues 5--9 and 11) removed approximately equal to 90% of both endogenous SLI and somatostatin added to plasma, but neither was removed by affinity chromatography on antibodies directed against the NH2-terminal region of somatostatin (residues 1--4). The SLI from plasma and from pancreas perfusate isolated by affinity chromatography was identical in molecular size, charge, and immunometric properties to synthetic somatostatin. It is concluded that endogenous SLI is secreted by the pancreas and stomach in a form not distinguishable from synthetic somatostatin, but circulates in plasma bound to large molecular weight components; the NH2-terminal residues of somatostatin appear to be important in this binding.

Animals↗