scholarly journals Immunocytochemical localization of ornithine transcarbamylase in rat intestinal mucosa. Light and electron microscopic study.

1988 ◽  
Vol 36 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Y Hamano ◽  
H Kodama ◽  
M Yanagisawa ◽  
Y Haraguchi ◽  
M Mori ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Small Intestine ◽  
Epithelial Cells ◽  
Light Microscopy ◽  
Intestinal Mucosa ◽  
Intestinal Epithelial Cells ◽  
Protein A ◽  
Intestinal Epithelial ◽  
Electron Microscopic ◽  
Small Intestinal

We investigated light and electron microscopic localization of ornithine transcarbamylase (OTC) in rat intestinal mucosa. In the immunoblotting assay of OTC-related protein, a single protein band with a molecular weight of about 36,500 is observed in extracts of liver and small intestinal mucosa but is not observed in those of stomach and large intestine. For light microscopy, tissue slices of the digestive system were embedded in Epon and stained by using anti-bovine OTC rabbit IgG and the immunoenzyme technique. For electron microscopy, slices of these and the liver tissues were embedded in Lowicryl K4M and stained by the protein A-gold technique. By light microscopy, the absorptive epithelial cells of duodenum, jejunum, and ileum stained positively for OTC, but stomach, large intestine, rectum, and propria mucosa of small intestine were not stained. Electron microscopy showed that gold particles representing the antigenic sites for OTC were confined to the mitochondrial matrix of hepatocytes and small intestinal epithelial cells. However, the enzyme was detected in mitochondria of neither liver endothelial cells, submucosal cells of small intestine, nor large intestinal epithelial cells. Labeling density of mitochondria in the absorptive epithelial cells of duodenum, jejunum, and ileum was about half of that in liver cells.

scholarly journals Small intestine barrier function failure induces systemic inflammation in monosodium glutamate-induced chronically obese mice

2019 ◽  
Vol 44 (6) ◽  
pp. 587-594 ◽  
Author(s):  
Kazuhiko Nakadate ◽  
Tomoya Hirakawa ◽  
Sawako Tanaka-Nakadate
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Systemic Inflammation ◽  
Intestinal Epithelial Cells ◽  
Monosodium Glutamate ◽  
Intestinal Epithelial ◽  
Obese Mice ◽  
Gastrointestinal Barrier ◽  
Small Intestinal ◽  
Functional Deterioration

Chronic obesity has increased worldwide, in conjunction with type 2 diabetes. Chronic obesity causes systemic inflammation that may result in functional deterioration of the gastrointestinal barrier. However, gastrointestinal conditions associated with chronic obesity have not been comprehensively investigated. The purpose of this study was to evaluate morphological changes in small intestine barrier structures during chronic obesity. A mouse model of chronic obesity induced by monosodium glutamate treatment was established. At postnatal week 15, pathological changes including in small intestinal epithelial cells were analyzed in chronically obese mice compared with controls. Numerous gaps were identified between small intestinal epithelial cells in chronically obese mice, and levels of both desmosomal and tight junction proteins were significantly lower in their small intestinal epithelial cells. Moreover, in chronically obese mice, a significant increase in the number of intestinal inflammatory cells, particularly macrophages, was observed; in addition, blood samples from the mouse model show an increase in markers of inflammation, tumor necrosis factor-alpha and interleukin-1-beta. These findings suggest that functional deterioration of adhesion structures between small intestinal epithelial cells causes gastrointestinal barrier function failure, leading to a rise in intestinal permeability to blood vessels and consequent systemic inflammation, characterized by macrophage infiltration.

Primary culture of salamander intestinal epithelial cells from nests: whole cell Na+ currents induced by valine

1994 ◽  
Vol 267 (1) ◽  
pp. G59-G66
Author(s):  
J. F. White
Keyword(s):  
Epithelial Cells ◽  
Intestinal Mucosa ◽  
Intestinal Epithelial Cells ◽  
Intestinal Cells ◽  
Small Intestinal Mucosa ◽  
Intestinal Epithelial ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Inward Current ◽  
Small Intestinal

Methods are described for isolating the cell nests, subepithelial clusters of germinative cells, from salamander intestinal mucosa and for growing the nests in culture into polarized monolayers of intestinal epithelial cells. Cells were viable in culture for up to 3 wk. The capacity of the monolayer cells to engage in membrane transport was evaluated using the patch-clamp technique in the whole cell mode. L-Valine (25 mM) induced an inward current in small intestinal cells of 25.8 +/- 5.7 pA and depolarized the cell membrane 14.5 +/- 1.6 mV. L-Alanine and L-phenylalanine were similarly effective, whereas D-valine was ineffective. The Km of the transporter for valine was 90 mM. Replacement of bath Na with tris(hydroxymethyl)aminomethane eliminated the inward current induced by valine. The basal (solute-independent) inward current was also reduced by Na+ replacement. Glucose did not induce a Na+ current. In contrast to the effect of valine on small intestinal cells, large intestinal cells were unresponsive to valine. It is concluded that the cultured small intestinal cells possess Na-amino acid but not Na-sugar cotransport. This profile of behavior is characteristic of undifferentiated small intestinal cells. Primary cultures of salamander small intestinal cells should be useful for studying enterocyte function and the developmental biology of the small intestinal mucosa.

Three-dimensional organization and functional relationships of endocytotic compartments in pig intestinal epithelial cells

1992 ◽  
Vol 50 (1) ◽  
pp. 576-577
Author(s):  
Julian P. Heath ◽  
Buford L. Nichols ◽  
László G. Kömüves
Keyword(s):  
Electron Microscopy ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Three Dimensional ◽  
Intestinal Epithelial ◽  
Cell Surfaces ◽  
Basal Surface ◽  
Functional Relationships

The newborn pig intestine is adapted for the rapid and efficient absorption of nutrients from colostrum. In enterocytes, colostral proteins are taken up into an apical endocytotic complex of channels that transports them to target organelles or to the basal surface for release into the circulation. The apical endocytotic complex of tubules and vesicles clearly is a major intersection in the routes taken by vesicles trafficking to and from the Golgi, lysosomes, and the apical and basolateral cell surfaces.Jejunal tissues were taken from piglets suckled for up to 6 hours and prepared for electron microscopy and immunocytochemistry as previously described.

scholarly journals Enterococcus faecium PNC01 isolated from the intestinal mucosa of chicken as an alternative for antibiotics to reduce feed conversion rate in broiler chickens

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Yang He ◽  
Xuan Liu ◽  
Yuanyang Dong ◽  
Jiaqi Lei ◽  
Koichi Ito ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Mucosa ◽  
Conversion Rate ◽  
Broiler Chickens ◽  
Intestinal Epithelial Cells ◽  
Relative Length ◽  
Intestinal Epithelial ◽  
Feed Conversion ◽  
Broiler Production ◽  
Feed Conversion Rate

Abstract Background The development and utilization of probiotics had many environmental benefits for replacing antibiotics in animal production. Bacteria in the intestinal mucosa have better adhesion to the host intestinal epithelial cells compared to bacteria in the intestinal contents. In this study, lactic acid bacteria were isolated from the intestinal mucosa of broiler chickens and investigated as the substitution to antibiotic in broiler production. Results In addition to acid resistance, high temperature resistance, antimicrobial sensitivity tests, and intestinal epithelial cell adhesion, Enterococcus faecium PNC01 (E. faecium PNC01) was showed to be non-cytotoxic to epithelial cells. Draft genome sequence of E. faecium PNC01 predicted that it synthesized bacteriocin to perform probiotic functions and bacteriocin activity assay showed it inhibited Salmonella typhimurium from invading intestinal epithelial cells. Diet supplemented with E. faecium PNC01 increased the ileal villus height and crypt depth in broiler chickens, reduced the relative length of the cecum at day 21, and reduced the relative length of jejunum and ileum at day 42. Diet supplemented with E. faecium PNC01 increased the relative abundance of Firmicutes and Lactobacillus, decreased the relative abundance of Bacteroides in the cecal microbiota. Conclusion E. faecium PNC01 replaced antibiotics to reduce the feed conversion rate. Furthermore, E. faecium PNC01 improved intestinal morphology and altered the composition of microbiota in the cecum to reduce feed conversion rate. Thus, it can be used as an alternative for antibiotics in broiler production to avoid the adverse impact of antibiotics by altering the gut microbiota. Graphic Abstract

scholarly journals miRNA-30e regulates abnormal differentiation of small intestinal epithelial cells in diabetic mice by downregulating Dll4 expression

2016 ◽  
Vol 49 (1) ◽  
pp. 102-114 ◽  
Author(s):  
Ti-Dong Shan ◽  
Hui Ouyang ◽  
Tao Yu ◽  
Jie-Yao Li ◽  
Can-Ze Huang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Diabetic Mice ◽  
Small Intestinal

scholarly journals Mitochondrial gene expression in small intestinal epithelial cells

1995 ◽  
Vol 308 (2) ◽  
pp. 665-671 ◽  
Author(s):  
T P Mayall ◽  
I Bjarnason ◽  
U Y Khoo ◽  
T J Peters ◽  
A J S Macpherson
Keyword(s):  
Epithelial Cells ◽  
Cytochrome Oxidase ◽  
Cytochrome B ◽  
Intestinal Epithelial Cells ◽  
Mitochondrial Gene ◽  
Cytochrome Oxidase I ◽  
Mrna Levels ◽  
Intestinal Epithelial ◽  
Mitochondrial Transcription Factor ◽  
Small Intestinal

Most mitochondrial genes are transcribed as a single large transcript from the heavy strand of mitochondrial DNA, and are subsequently processed into the proximal mitochondrial (mt) 12 S and 16 S rRNAs, and the more distal tRNAs and mRNAs. We have shown that in intestinal epithelial biopsies the steady-state levels of mt 12 S and 16 S rRNA are an order of magnitude greater than those of mt mRNAs. Fractionation of rat small intestinal epithelial cells on the basis of their maturity has shown that the greatest ratios of 12 S mt rRNA/cytochrome b mt mRNA or 12 S mt rRNA/cytochrome oxidase I mt mRNA are found in the surface mature enterocytes, with a progressive decrease towards the crypt immature enteroblasts. Cytochrome b and cytochrome oxidase I mt mRNA levels are relatively uniform along the crypt-villus axis, but fractionation experiments showed increased levels in the crypt base. The levels of human mitochondrial transcription factor A are also greater in immature crypt enteroblasts compared with mature villus enterocytes. These results show that the relative levels of mt rRNA and mRNA are distinctly regulated in intestinal epithelial cells according to the crypt-villus position and differentiation status of the cells, and that there are higher mt mRNA and mt TFA levels in the crypts, consistent with increased transcriptional activity during mitochondrial biogenesis in the immature enteroblasts.

Effect of leptin on intestinal apolipoprotein AIV in response to lipid feeding

2001 ◽  
Vol 281 (3) ◽  
pp. R753-R759 ◽  
Author(s):  
Takashi Doi ◽  
Min Liu ◽  
Randy J. Seeley ◽  
Stephen C. Woods ◽  
Patrick Tso
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Regional Distribution ◽  
Intestinal Epithelial ◽  
Lipid Infusion ◽  
Intraduodenal Infusion ◽  
Crypt Cells

We determined apolipoprotein AIV (apo AIV) content in intestinal epithelial cells using immunohistochemistry when leptin was administered intravenously. Most of the apo AIV immunoreactivity in the untreated intestine was located in the villous cells as opposed to the crypt cells. Regional distribution of apo AIV immunostaining revealed low apo AIV content in the duodenum and high content in the jejunum that gradually decreases caudally toward the ileum. Intraduodenal infusion of lipid (4 h) significantly increased apo AIV immunoreactivity in the jejunum and ileum. Simultaneous intravenous leptin infusion plus duodenal lipid infusion markedly suppressed apo AIV immunoreactivity. Duodenal lipid infusion increased plasma apo AIV significantly (measured by ELISA), whereas simultaneous leptin infusion attenuated the increase. These findings suggest that leptin may regulate circulating apo AIV by suppressing apo AIV synthesis in the small intestine.

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