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At least 703 records · Page 39Linked to original sources
PubMed1987

[Fatty acid pattern in children with mucoviscidosis in relation to the degree of exocrine pancreas insufficiency].

Fatty acid composition were determined by gas chromatography in serum triglycerides and cholesterol esters of 32 patients (aged 7-17 years) with cystic fibrosis. According to their exocrine pancreas function (determined with secretin-cholecystokinin test), patients were divided in 3 groups. In comparison with previously measured values in 30 metabolically healthy children, patients with cystic fibrosis showed a significantly increased level of palmitic, palmitoleic, stearic, oleic, and linolenic acid in the triglyceride fraction and a significantly increased level of myristic, myristoleic, palmitoleic, stearic, oleic, and triene acid in the cholesterol ester fraction. However, in both fractions, concentration of linoleic acid was significantly decreased. It seems unlikely that malabsorption of ingested fat is responsible for the abnormalities in fatty acid pattern, because no significant differences could be found between the 3 patient's groups.

Adolescent↗
PubMedDate not supplied

Inspissation of pancreatic zymogen material in cystic fibrosis.

Cystic fibrosis is characterized by the elaboration of abnormal, thick, tenacious mucus resulting in obstructive disease in sites such as the lung and pancreas. In the pancreas, acinar plugs of mucus have been reported as the earliest recognizable morphologic lesion in cystic fibrosis. Since mucus is not normally elaborated within the pancreatic lobular tissue, the mechanism of accumulation of mucus in acini is enigmatic. To investigate this phenomenon, well-preserved autopsy pancreatic tissue was studied ultrastructurally. This study demonstrated very prominent mucous metaplasia in these diseased organs. Acinar plugs, though, developed before mucous metaplasia. Subsequent histochemical study was performed, which demonstrated that the early acinar plugs exhibited the same staining properties as zymogen granules and were distinct from the staining pattern of mucus in pancreatic tissue of cystic fibrosis patients. These findings, then, indicate that zymogen material, not mucus, becomes inspissated in the acini of the pancreas in early cystic fibrosis, and that subsequent mucous metaplasia occurs as the obstruction and exocrine atrophy progress.

Child↗
PubMedDate not supplied

The pancreatic duct cell: proliferative capabilities, specific characteristics, metaplasia, isolation, and culture.

The pancreatic duct cell, although a minor cell type of the pancreas, plays an important role in fluid/electrolyte and mucin secretion, and has been implicated in the development of pancreatic cancer, alcoholic pancreatitis, and cystic fibrosis. In the normal pancreas, the duct cell has the same low proliferative rate as acinar and endocrine cells. Under certain pathological circumstances, duct cells, as well as acinar and islet cells, may be stimulated to proliferate more rapidly. Pancreatic duct cells exhibit certain features not shared by acinar and/or endocrine cells, including a variety of antigens, mucins, enzymes, and morphological features. Adult duct cells resemble fetal pancreatic duct-like cells morphologically, but they have differentiated to at least a limited extent from their precursor cell type. Although there is no evidence that duct cells differentiate into acinar cells after pancreatic morphogenesis is complete, some islet cells develop from duct epithelium in the early postnatal period. Some pathological conditions may lead to the postnatal formation of islet cells from duct cells and may cause acinar cells to become duct-like in morphology or to die and be replaced by duct cells. A better understanding of duct cells is now possible because of the development of techniques for their isolation and culture free from other cell types. Several such techniques are reviewed.

Animals↗
PubMed1996

Plasma immunoreactive cationic trypsin(ogen) pattern in reserpinized rat model of cystic fibrosis. Resemblance to humans.

Plasma immunoreactive cationic trypsin (ogen) is elevated in cystic fibrosis during early infancy, before exocrine pancreatic insufficiency is fully developed. The recently developed cystic fibrosis mouse model carrying a mutated gene presents only minor pathologic findings in the pancreas. However, the reserpinized rat model shows cystic fibrosis-like defects in various exocrine glands, including the exocrine pancreas. Plasma immunoreactive cationic trypsin (ogen) has not been studied yet in this model. The present study explored the plasma immunoreactive cationic trypsin (ogen) pattern and possible mechanisms in this rat model. Plasma immunoreactive cationic trypsin (ogen) (RIA), pancreatic juice volume, protein, and trypsin, and pancreas weight were determined in rats treated with reserpine (0.5 mg/kg/day subcutaneously) for four or seven days, following cerulein stimulation (5 micrograms/kg/dose intraperitoneally), versus pair-fed controls. The first of four consecutive 30 min periods revealed peak values in all parameters. Four-day reserpine-treated rats demonstrated significantly higher plasma immunoreactive cationic trypsin (ogen) levels (167.3 +/- 12.8 vs 88.9 +/- 6.1 ng/ml; P < 0.0001) with similar values of pancreatic juice trypsin (8.2 +/- 2.4 vs 6.6 +/- 1.8 units/mg protein; P = NS) and volume (5.6 +/- 1.3 vs 4.2 +/- 1.6 mg/min/g pancreas; P = NS), compared to controls. Rats treated with reserpine for seven days revealed significantly lower values of plasma immunoreactive cationic trypsin (ogen) (39.2 +/- 8.4 vs 66.8 +/- 4.9 ng/ml; P < 0.001), pancreatic juice trypsin (1.9 +/- 0.3 vs 3.2 +/- 0.9 units/mg protein; P < 0.001) and volume (1.6 +/- 0.7 vs 3.1 +/- 0.6 mg/min/g pancreas; P < 0.001) compared to controls. We conclude that the reserpinized rat model resembles human cystic fibrosis as to elevated plasma immunoreactive cationic trypsin (ogen) before exocrine pancreatic insufficiency is fully developed. Since exocrine pancreatic volume secretion is intact at this stage, the mechanism of elevated plasma immunoreactive cationic trypsin is probably not due to ductular obstruction. We suggest that this model be studied further in order to investigate other possible mechanisms.

Analysis of Variance↗
PubMed1985

X-ray microanalysis of exocrine glands in animal models for cystic fibrosis.

Elemental distribution and ultrastructure of the submandibular gland, the parotid gland and the pancreas were investigated in three suggested animal models of the disease cystic fibrosis: the chronically reserpinized rat, the chronically isoproterenol-treated rat, and the chronically pilocarpine-treated rat. To elucidate the cellular mechanism underlying the effects of these treatments, chronic effects of specific alpha - and beta -adrenergic agonists, as well as acute effects of reserpine and various agonists were also investigated. Reserpine, isoproterenol, and pilocarpine cause an increase in the calcium concentration in submandibular gland acinar cells, due to an increased calcium content of the intracellular mucus. In the parotid gland, reserpine and isoproterenol cause a decrease of the calcium concentration in acinar cells, due to a lower calcium content of the zymogen granules. In the submandibular gland, a decreased cellular Na concentration was noted after chronic treatment with isoproterenol or pilocarpine, and after a single dose of reserpine or isoproterenol. Ultrastructural changes in the exocrine glands investigated included excessive accumulation of intracellular secretory material and formation of abnormal uncondensed secretion granules. A common pattern in the 'animal models' appears to be (1) inhibition of secretion resulting in intracellular accumulation of secretory material, (2) synthesis of secretory macromolecules with altered cation-binding properties.

Adrenergic beta-Agonists↗