Effect of vitamin B6 deficiency on pancreatic acinar cell function

Life Sciences ◽  
1980 ◽  
Vol 26 (9) ◽  
pp. 715-724 ◽  
Author(s):  
Manjit Singh
Keyword(s):  
Acinar Cell ◽  
Vitamin B6 ◽  
Cell Function ◽  
Pancreatic Acinar Cell ◽  
Vitamin B6 Deficiency

scholarly journals SEC23B is required for pancreatic acinar cell function in adult mice

2017 ◽  
Vol 28 (15) ◽  
pp. 2146-2154 ◽  
Author(s):  
Rami Khoriaty ◽  
Nancy Vogel ◽  
Mark J. Hoenerhoff ◽  
M. Dolors Sans ◽  
Guojing Zhu ◽  
...  
Keyword(s):  
Acinar Cell ◽  
Cell Function ◽  
Acinar Cells ◽  
Cell Loss ◽  
Normal Function ◽  
Pancreatic Acinar Cell ◽  
Pancreatic Acinar Cells ◽  
Total Protein Content ◽  
Pancreatic Cell ◽  
Adult Mice

Mice with germline absence of SEC23B die perinatally, exhibiting massive pancreatic degeneration. We generated mice with tamoxifen-inducible, pancreatic acinar cell–specific Sec23b deletion. Inactivation of Sec23b exclusively in the pancreatic acinar cells of adult mice results in decreased overall pancreatic weights from pancreatic cell loss (decreased pancreatic DNA, RNA, and total protein content), as well as degeneration of exocrine cells, decreased zymogen granules, and alterations in the endoplasmic reticulum (ER), ranging from vesicular ER to markedly expanded cisternae with accumulation of moderate-density content or intracisternal granules. Acinar Sec23b deletion results in induction of ER stress and increased apoptosis in the pancreas, potentially explaining the loss of pancreatic cells and decreased pancreatic weight. These findings demonstrate that SEC23B is required for normal function of pancreatic acinar cells in adult mice.

Cholecystokinin and regulation of pancreatic acinar cell function

1993 ◽  
Vol 73 (4) ◽  
pp. 701-723 ◽  
Author(s):  
J. A. Williams ◽  
G. T. Blevins
Keyword(s):  
Acinar Cell ◽  
Cell Function ◽  
Pancreatic Acinar Cell

In vivo rat pancreatic acinar cell function during supramaximal stimulation with caerulein

1985 ◽  
Vol 249 (6) ◽  
pp. G702-G710 ◽  
Author(s):  
A. Saluja ◽  
I. Saito ◽  
M. Saluja ◽  
M. J. Houlihan ◽  
R. E. Powers ◽  
...  
Keyword(s):  
Acinar Cell ◽  
Intracellular Transport ◽  
Cell Function ◽  
Acinar Cells ◽  
Pancreatic Acinar Cell ◽  
Zymogen Granule ◽  
Zymogen Granules ◽  
Morphological Studies ◽  
Supramaximal Stimulation

Infusion of a supramaximal dose of caerulein results in acute interstitial pancreatitis in rats. We report studies of in vivo pancreatic acinar cell function during the initial 3.5 h of supramaximal stimulation with caerulein (5 micrograms X kg-1 X h-1). Amino acid [( 3H]phenylalanine) uptake was not altered, and there was no change in the rate or extent of protein synthesis or in intracellular transport of in vivo pulse-labeled proteins from microsome to zymogen granule-enriched fractions. However, the discharge of labeled protein was markedly inhibited. Radioautographic studies indicated that the pulse-labeled proteins retained in the gland were not located extracellularly but had accumulated within acinar cells, with a preferential distribution at the cell apex (presumably in zymogen granules) and in large vacuoles that form within the cell during hyperstimulation. Supramaximal stimulation with caerulein also caused increasing amounts of amylase and labeled proteins to be recovered in the postmicrosomal fraction. These findings suggest that supramaximal stimulation causes digestive enzymes to become localized in organelles that are fragile and subject to disruption during tissue homogenization. These organelles may be the vacuoles noted in morphological studies and believed to represent immature condensing vacuoles and/or crinophagic vacuoles.

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