Fat-induced changes of the integrity of rat exocrine pancreas measured in vivo and in vitro

1998 ◽  
Vol 114 ◽  
pp. A448
Author(s):  
P. Chowdhury ◽  
M. Nishikawa ◽  
G.T. Blevins ◽  
P.L. Rayford
Keyword(s):  
Exocrine Pancreas ◽  
Rat Exocrine Pancreas ◽  
Induced Changes

Effects of in vivo cholinergic stimulation of rat exocrine pancreas

1983 ◽  
Vol 244 (6) ◽  
pp. G623-G629
Author(s):  
G. Adler ◽  
G. Gerhards ◽  
J. Schick ◽  
G. Rohr ◽  
H. F. Kern
Keyword(s):  
Dose Response ◽  
Exocrine Pancreas ◽  
Pancreatic Enzyme ◽  
Target Cells ◽  
Response Curves ◽  
Cholinergic Agent ◽  
Rat Exocrine Pancreas ◽  
Biphasic Dose Response

Peptide and cholinergic secretagogues both produce biphasic dose-response curves for pancreatic enzyme secretion in vitro: supraoptimal doses result in submaximal secretory responses. We compared the effects of maximal and supramaximal doses of a cholinergic agent (carbachol) on rat exocrine pancreas in vivo. In conscious rats, volume and enzyme output were measured from the cannulated pancreatic duct during infusion of carbachol for 3 h. Infusion of 5 X 10(-7) mol . kg-1 . h-1 carbachol caused optimal stimulation, whereas a supraoptimal dose (5 X 10(-6) mol . kg-1 . h-1) resulted in submaximal response. Similar results were achieved when discharge of amylase and protein synthesis was determined in vitro after carbachol in vivo. Supraoptimal doses of carbachol increased serum amylase and enhanced acinar cell lysosomal activity in the Golgi area. The latter appeared to induce fusion of zymogen granules, which resulted in cytoplasmic vacuoles. The in vivo results corroborate in vitro findings of a biphasic dose-response relationship for carbachol and demonstrate destructive effects of supraoptimal concentrations on target cells.

Nonparallel secretion of GP-2 from exocrine pancreas implies luminal coupling between acinar and duct cells

1994 ◽  
Vol 267 (1) ◽  
pp. G40-G51 ◽  
Author(s):  
S. D. Freedman ◽  
K. Sakamoto ◽  
G. A. Scheele
Keyword(s):  
Exocrine Pancreas ◽  
Acinar Cells ◽  
Zymogen Granule ◽  
Zymogen Granules ◽  
Pancreatic Acini ◽  
Glycosyl Phosphatidylinositol ◽  
Cellular Processes ◽  
Rat Exocrine Pancreas

The in vivo and in vitro secretion of glycoprotein-2 (GP-2), a glycosyl phosphatidylinositol (GPI)-anchored protein from the rat exocrine pancreas, was characterized. GP-2 was secreted in a nonparallel manner compared with amylase, a marker of secretory enzymes. Attenuated GP-2 secretion correlated with hormones that stimulated exocytosis in acinar cells. Augmented GP-2 secretion correlated with hormones that stimulated fluid and bicarbonate secretion from ductal elements. Immunofluorescence studies identified an enriched pool of GP-2 tightly bound to the apical membranes of acinar cells in addition to zymogen granules. This non-zymogen granule pool appears to represent the source of GP-2 released from acinar cells in a nonparallel manner. With the use of dispersed pancreatic acini largely devoid of ductal elements, GP-2 release was found to be augmented by alkaline pH. Thus GP-2 secretion appears to be modulated by two discrete cellular processes: 1) delivery of prereleased GP-2 within zymogen granules to the ductal lumen by exocytic mechanisms and 2) enzymatic release of GPI-anchored GP-2 from the luminal membranes, a kinetic process that appears to be regulated by secretin- or carbachol-induced secretion of bicarbonate.

scholarly journals Insulin induces rapid and specific rearrangement of the cytoskeleton of rat mesangial cells in vitro.

1996 ◽  
Vol 44 (2) ◽  
pp. 91-101 ◽  
Author(s):  
A K Berfield ◽  
G J Raugi ◽  
C K Abrass
Keyword(s):  
Mesangial Cells ◽  
Focal Adhesions ◽  
Cytoskeletal Proteins ◽  
Direct Effects ◽  
Ligand Effects ◽  
Igf I ◽  
Induced Changes ◽  
Secondary Ligand

Mesangial cells (MCs) grown without supplemental insulin (SI-MCs) express a quiescent phenotype and extracellular matrix (ECM) composition similar to MCs in vivo. In contrast, MCs routinely propagated in insulin (SI+MCs) are stimulated to proliferate, change their phenotype, and produce large amounts of collagens I and III. These effects of insulin may in part be mediated through cytoskeletal rearrangement. Differences in cytoskeletal arrangement were compared between SI-MCs and SI+MCs and 1 hr after addition of insulin (1 nM) or IGF-1 (100 nM) to SI-MCs. Cells were examined by light microscopy, electron microscopy, and immunostaining for specific cytoskeletal proteins and fibronectin. Insulin induced rapid rearrangement of stress fibers. Surface ruffling, actin aggregation, vimentin retraction, rearrangement of vinculin in focal adhesions, and fibronectin extraction were apparent. These direct effects of insulin on the SI-MC cytoskeleton occurred before insulin-induced changes in ECM composition. IGF-I induced cytoskeletal reorganization distinct from insulin. These observations demonstrate that insulin and IGF-I have unique effects on the MC cytoskeleton, which is turn may mediate secondary ligand effects on MCs.

scholarly journals Suppressed expression of genes involved in transcription and translation in in vitro compared with in vivo cultured bovine embryos

Reproduction ◽  
2006 ◽  
Vol 131 (4) ◽  
pp. 651-660 ◽  
Author(s):  
D Corcoran ◽  
T Fair ◽  
S Park ◽  
D Rizos ◽  
O V Patel ◽  
...  
Keyword(s):  
Expressed Sequence Tags ◽  
Differentially Expressed ◽  
Bovine Embryos ◽  
Quantitative Real Time Pcr ◽  
Expression Of Genes ◽  
Mrna Transcripts ◽  
Induced Changes ◽  
Expressed Sequence

In vivo-derived bovine embryos are of higher quality than those derivedin vitro. Many of the differences in quality can be related to culture environment-induced changes in mRNA abundance. The aim of this study was to identify a range of mRNA transcripts that are differentially expressed between bovine blastocysts derived fromin vitroversusin vivoculture. Microarray (BOTL5) comparison betweenin vivo- andin vitro-cultured bovine blastocysts identified 384 genes and expressed sequence tags (ESTs) that were differentially expressed; 85% of these were down-regulated inin vitrocultured blastocysts, showing a much reduced overall level of mRNA expression inin vitro- compared within vivo-cultured blastocysts. Relative expression of 16 out of 23 (70%) differentially expressed genes (according toPvalue) were verified in new pools ofin vivo- andin vitro-cultured blastocysts, using quantitative real-time PCR. Most (10 out of 16) are involved in transcription and translation events, suggesting that the reason whyin vitro-derived embryos are of inferior quality compared within vivo-derived embryos is due to a deficiency of the machinery associated with transcription and translation.

Role of endothelial cells in regulating hemoglobin-induced changes in lymphatic pumping

1992 ◽  
Vol 263 (6) ◽  
pp. H1880-H1887 ◽  
Author(s):  
R. M. Elias ◽  
J. Eisenhoffer ◽  
M. G. Johnston
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Inhibitory Effect ◽  
Direct Inhibitory Effect ◽  
Induced Changes ◽  
Lymphatic Pumping ◽  
Pumping Activity

Studies with a sheep isolated duct preparation in vivo demonstrated that the route of administration of hemoglobin was important in demonstrating its inhibitory effect on lymphatic pumping. With autologous oxyhemoglobin administered intravenously (final plasma concentration 5 x 10(-5) M), pumping was not inhibited. However, the addition of oxyhemoglobin (5 x 10(-5) M) into the reservoir (lumen of the duct) resulted in > 95% inhibition of pumping. The extraluminal administration of oxyhemoglobin (10(-5) M) to bovine mesenteric lymphatics in vitro resulted in a 40% inhibition of pumping, whereas the introduction of oxyhemoglobin (10(-5) M) into the lumen of the vessels suppressed pumping 95%. In vessels mechanically denuded of endothelium, intraluminal oxyhemoglobin inhibited pumping 50%. These results suggested that oxyhemoglobin depressed pumping through an effect on both smooth muscle and endothelium. Once pumping was inhibited with oxyhemoglobin administration, stimulation of the duct with elevations in transmural pressure restored pumping activity when endothelial cells were present. However, in the absence of endothelium, pumping decreased with increases in distending pressures. We conclude that oxyhemoglobin has a direct inhibitory effect on lymphatic smooth muscle. The ability of oxyhemoglobin to alter the pressure range over which the lymph pump operates appears to be dependent on an intact endothelium.

Changes in the exocrine pancreas secondary to altered small intestinal function in the CF mouse

2001 ◽  
Vol 281 (4) ◽  
pp. G899-G906 ◽  
Author(s):  
Robert C. De Lisle ◽  
Kathryn S. Isom ◽  
Donna Ziemer ◽  
Calvin U. Cotton
Keyword(s):  
Exocrine Pancreas ◽  
Exocrine Function ◽  
Amylase Secretion ◽  
Mrna Levels ◽  
Intestinal Function ◽  
Small Intestinal ◽  
First Time ◽  
Camp Levels

The exocrine pancreas of the cystic fibrosis (CF) mouse ( cftrm1UNC ) is only mildly affected compared with the human disease, providing a useful model to study alterations in exocrine function. The CF mouse pancreas has ∼50% of normal amylase levels and ∼200% normal Muclin levels, the major sulfated glycoprotein of the pancreas. Protein biosynthetic rates and mRNA levels for amylase were not altered in CF compared with normal mice, and increases in Muclin biosynthesis and mRNA paralleled the increased protein content. Stimulated pancreatic amylase secretion in vitro and in vivo tended to be increased in CF mice but was not statistically significant compared with normal mice. We show for the first time that the CF mouse duodenum is abnormally acidic (normal intestinal pH = 6.47 ± 0.05; CF intestinal pH = 6.15 ± 0.07) and hypothesize that this may result in increased signaling to the exocrine pancreas. There were significant increases in CF intestinal mRNA levels for secretin (310% of normal, P < 0.001) and vasoactive intestinal peptide (148% of normal, P < 0.05). Furthermore, CF pancreatic cAMP levels were 147% of normal ( P < 0.01). These data suggest that the CF pancreas may be chronically stimulated by cAMP-mediated signals, which in turn may exacerbate protein plugging in the acinar/ductal lumen, believed to be the primary cause of destruction of the pancreas in CF.

scholarly journals Transendothelial movement of adiponectin is restricted by glucocorticoids

2017 ◽  
Vol 234 (2) ◽  
pp. 101-114 ◽  
Author(s):  
Thanh Q Dang ◽  
Nanyoung Yoon ◽  
Helen Chasiotis ◽  
Emily C Dunford ◽  
Qilong Feng ◽  
...  
Keyword(s):  
Critical Role ◽  
Endothelial Permeability ◽  
The Body ◽  
Diabetic Rat ◽  
Mrna Levels ◽  
Endothelial Monolayers ◽  
Basolateral Side ◽  
Induced Changes

Altered permeability of the endothelial barrier in a variety of tissues has implications both in disease pathogenesis and treatment. Glucocorticoids are potent mediators of endothelial permeability, and this forms the basis for their heavily prescribed use as medications to treat ocular disease. However, the effect of glucocorticoids on endothelial barriers elsewhere in the body is less well studied. Here, we investigated glucocorticoid-mediated changes in endothelial flux of Adiponectin (Ad), a hormone with a critical role in diabetes. First, we used monolayers of endothelial cells in vitro and found that the glucocorticoid dexamethasone increased transendothelial electrical resistance and reduced permeability of polyethylene glycol (PEG, molecular weight 4000 Da). Dexamethasone reduced flux of Ad from the apical to basolateral side, measured both by ELISA and Western blotting. We then examined a diabetic rat model induced by treatment with exogenous corticosterone, which was characterized by glucose intolerance and hyperinsulinemia. There was no change in circulating Ad but less Ad protein in skeletal muscle homogenates, despite slightly higher mRNA levels, in diabetic vs control muscles. Dexamethasone-induced changes in Ad flux across endothelial monolayers were associated with alterations in the abundance of select claudin tight junction (TJ) proteins. shRNA-mediated knockdown of one such gene, claudin-7, in HUVEC resulted in decreased TEER and increased adiponectin flux, confirming the functional significance of Dex-induced changes in its expression. In conclusion, our study identifies glucocorticoid-mediated reductions in flux of Ad across endothelial monolayers in vivo and in vitro. This suggests that impaired Ad action in target tissues, as a consequence of reduced transendothelial flux, may contribute to the glucocorticoid-induced diabetic phenotype.

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