Demonstration of methionine synthetase in intestinal mucosal cells of the rat

1985 ◽  
Vol 69 (3) ◽  
pp. 287-292 ◽  
Author(s):  
J. N. Keating ◽  
D. G. Weir ◽  
J. M. Scott
Keyword(s):  
Crypt Cell ◽  
Cell Populations ◽  
Buffer System ◽  
Mucosal Cell ◽  
Mucosal Cells ◽  
Rat Duodenum ◽  
Small Intestinal ◽  
Intestinal Mucosal Cells ◽  
Crypt Cells

1. Methionine synthetase was measured in the mucosal cells of the rat duodenum, jejunum and ileum by a previously employed method for mucosal cell isolation. No activity was found in these cells. 2. When a dual buffer system for the isolation of villous and crypt cell population was substituted, however, methionine synthetase was found to be active in the duodenum, jejunum and ileum, both in the villous and crypt cell populations. The activity was significantly higher in the crypt cells than in the villous cells throughout the intestine, and higher levels were found in the ileum than in the duodenum or jejunum. 3. As had been previously reported for the rat liver, nitrous oxide in vivo reduced the enzyme activity in both the villous and crypt cell populations, suggesting a role in vivo for the enzyme. We conclude that methionine synthetase is both present and active in the small intestinal mucosal cells of the rat.

Bacterial-Mucosal Cell Junctional Complexes

1974 ◽  
Vol 32 ◽  
pp. 144-145
Author(s):  
Roger C. Wagner
Keyword(s):  
Intestinal Wall ◽  
Rat Colon ◽  
Mucosal Cell ◽  
Gram Negative Bacteria ◽  
Gram Negative ◽  
Mucosal Cells ◽  
Mucosal Lining ◽  
Degenerative Alterations ◽  
Junctional Complexes ◽  
Intestinal Mucosal Cells

Bacteria exhibit the ability to adhere to the apical surfaces of intestinal mucosal cells. These attachments either precede invasion of the intestinal wall by the bacteria with accompanying inflammation and degeneration of the mucosa or represent permanent anchoring sites where the bacteria never totally penetrate the mucosal cells.Endemic gram negative bacteria were found attached to the surface of mucosal cells lining the walls of crypts in the rat colon. The bacteria did not intrude deeper than 0.5 urn into the mucosal cells and no degenerative alterations were detectable in the mucosal lining.

Fine Structural Localization of Acyltransferases Involved in Lipid Synthesis in Intestinal Mucosa.

1970 ◽  
Vol 28 ◽  
pp. 54-55
Author(s):  
R. J. Barrnett ◽  
J. A. Higgins
Keyword(s):  
Smooth Endoplasmic Reticulum ◽  
Lipid Synthesis ◽  
Mucosal Cell ◽  
Structural Localization ◽  
Morphological Studies ◽  
Mucosal Cells ◽  
Initial Appearance ◽  
Sh Group ◽  
Hydrolysis Of ◽  
Intestinal Mucosal Cells

The main products of intestinal hydrolysis of dietary triglycerides are free fatty acids and monoglycerides. These form micelles from which the lipids are absorbed across the mucosal cell brush border. Biochemical studies have indicated that intestinal mucosal cells possess a triglyceride synthesising system, which uses monoglyceride directly as an acylacceptor as well as the system found in other tissues in which alphaglycerophosphate is the acylacceptor. The former pathway is used preferentially for the resynthesis of triglyceride from absorbed lipid, while the latter is used mainly for phospholipid synthesis. Both lipids are incorporated into chylomicrons. Morphological studies have shown that during fat absorption there is an initial appearance of fat droplets within the cisternae of the smooth endoplasmic reticulum and that these subsequently accumulate in the golgi elements from which they are released at the lateral borders of the cell as chylomicrons.We have recently developed several methods for the fine structural localization of acyltransferases dependent on the precipitation, in an electron dense form, of CoA released during the transfer of the acyl group to an acceptor, and have now applied these methods to a study of the fine structural localization of the enzymes involved in chylomicron lipid biosynthesis. These methods are based on the reduction of ferricyanide ions by the free SH group of CoA.

scholarly journals Effects of cholecalciferol on the translocation of calcium by non-everted ileum in vitro

1975 ◽  
Vol 152 (2) ◽  
pp. 181-190 ◽  
Author(s):  
Eric S. Holdsworth ◽  
John E. Jordan ◽  
Ellen Keenan
Keyword(s):  
Sodium Dodecyl ◽  
Electrical Potential ◽  
Basement Membranes ◽  
Metabolic Energy ◽  
Temperature Sensitive ◽  
Mucosal Cell ◽  
Electrical Potential Difference ◽  
Mucosal Cells

An apparatus is described that allows perfusion of a non-everted segment of intestine in vitro and the study of the accumulation of substances within the mucosal cells. The translocation of Ca2+ by rachitic-chick ileum and the effect of pretreatment with cholecalciferol was investigated, with the following conclusions. (1) Entry of Ca2+ across the microvilli into mucosal cells is by diffusion; it does not require metabolic energy or the presence of any other inorganic ions. (2) Pretreatment of the chick with cholecalciferol causes increased permeability of the microvillus to Ca2+ in both directions (lumen to cell, cell to lumen). The increased transport brought about by cholecalciferol in vivo can be partially mimicked by sodium dodecyl sulphate added in vitro. (3) The sign and the magnitude of the electrical potential difference prevailing across the ileum does not influence Ca2+ transport. (4) Exit of Ca2+ from the mucosal cell is temperature-sensitive, requires metabolic energy and Na+. (5) Pretreatment with cholecalciferol caused increased movement of Ca2+ out of the cell across the basement membranes. This effect of cholecalciferol given in vivo could be markedly increased by the presence of dicyclohexylcarbodi-imide in the perfusion fluid. These observations suggested that cholecalciferol increased Ca2+ entry (and exit) at the mucosal surface and also caused Ca2+ to be more available to the pump at the serosal surface.

Localization of HLA and IA Antigens and β2 Microglobulins in Human Small Intestinal Mucosal Cells

1983 ◽  
Vol 64 (2) ◽  
pp. 69P-69P
Author(s):  
C. O'Morain ◽  
F. Ameglio ◽  
R. Tosi ◽  
S. Auricchio ◽  
S. Cucchiara ◽  
...  
Keyword(s):  
Ia Antigens ◽  
Mucosal Cells ◽  
Small Intestinal ◽  
Intestinal Mucosal Cells

scholarly journals Rack1 function in intestinal epithelia: regulating crypt cell proliferation and regeneration and promoting differentiation and apoptosis

2018 ◽  
Vol 314 (1) ◽  
pp. G1-G13 ◽  
Author(s):  
Zhuan-Fen Cheng ◽  
Reetesh K. Pai ◽  
Christine A. Cartwright
Keyword(s):  
Cell Proliferation ◽  
Paneth Cell ◽  
Cell Cycle Checkpoints ◽  
Crypt Cell ◽  
Colon Cells ◽  
Intestinal Epithelia ◽  
Crypt Cell Proliferation ◽  
Crypt Cells

Previously, we showed that receptor for activated C kinase 1 (Rack1) regulates growth of colon cells in vitro, partly by suppressing Src kinase activity at key cell cycle checkpoints, in apoptotic and cell survival pathways and at cell-cell adhesions. Here, we generated mouse models of Rack1 deficiency to assess Rack1’s function in intestinal epithelia in vivo. Intestinal Rack1 deficiency resulted in proliferation of crypt cells, diminished differentiation of crypt cells into enterocyte, goblet, and enteroendocrine cell lineages, and expansion of Paneth cell populations. Following radiation injury, the morphology of Rack1-deleted small bowel was strikingly abnormal with development of large polypoid structures that contained many partly formed villi, numerous back-to-back elongated and regenerating crypts, and high-grade dysplasia in surface epithelia. These abnormalities were not observed in Rack1-expressing areas of intestine or in control mice. Following irradiation, apoptosis of enterocytes was strikingly reduced in Rack1-deleted epithelia. These novel findings reveal key functions for Rack1 in regulating growth of intestinal epithelia: suppressing crypt cell proliferation and regeneration, promoting differentiation and apoptosis, and repressing development of neoplasia. NEW & NOTEWORTHY Our findings reveal novel functions for receptor for activated C kinase 1 (Rack1) in regulating growth of intestinal epithelia: suppressing crypt cell proliferation and regeneration, promoting differentiation and apoptosis, and repressing development of neoplasia.

scholarly journals Effects of dietary iron deficiency and tungsten supplementation on59Fe absorption and gastricretention from59Fe compounds in rats

1989 ◽  
Vol 61 (3) ◽  
pp. 573-581 ◽  
Author(s):  
Gillian E. Shears ◽  
R. J. Neale ◽  
D. A. Ledward
Keyword(s):  
Iron Deficiency ◽  
Xanthine Oxidase ◽  
Gastric Retention ◽  
Dietary Iron ◽  
Digestion Time ◽  
Mucosal Cells ◽  
Ferroxidase Activity ◽  
Intestinal Mucosal Cells ◽  
Absorption Characteristics

1. In vivo59Fe absorption from intrinsically labelled Fe-containing fractions of liver and blood were measured in rats by intragastric dosing. All rats were fed on a low-Fe diet for 3 d before dosing in order to standardize the Fe status of the intestinal mucosal cells.2. An increase in digestion time from 2 to 12 h increased59Fe absorption (P< 0.01) from all fractions except ferritin.3. Fe-deficient rats when compared with essentially Fe-replete rats showed decreased gastric retention for all fractions, but increased59Fe absorption over 2 h only from ferritin. Ferritin showed several unusual absorption characteristics.4. Dietary tungsten supplementation of Fe-deficient rats reduced the ferroxidase activity of intestinal mucosal xanthine oxidase. In addition, gastric retention and59Fe absorption (P< 0.05) from all fractions were increased.

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