scholarly journals Morphology of small intestinal mucosa and intestinal weight change with metabolic type of cattle

2008 ◽  
Vol 53 (No. 10) ◽  
pp. 525-532 ◽  
Author(s):  
R. Zitnan ◽  
J. Voigt ◽  
S. Kuhla ◽  
J. Wegner ◽  
A. Chudy ◽  
...  
Keyword(s):  
Body Weight ◽  
Small Intestine ◽  
Intestinal Mucosa ◽  
High Energy ◽  
Proximal Jejunum ◽  
Small Intestinal Mucosa ◽  
Apparent Digestibility ◽  
Cattle Breeds ◽  
Metabolic Type ◽  
Small Intestinal

The objective of this study was to investigate rumen fermentation, apparent digestibility of nutrients, and morphology of ruminal und intestinal mucosa in two cattle breeds of different metabolic type. From each breed six purebred German Holstein (H) bulls representing the secretion type and six Charolais (CH) bulls representing the accretion type were raised and fattened under identical conditions with <I>semi ad libitum</I> feeding of a high energy diet. The animals were used for a digestion trial started at nine months of age and animals were slaughtered at 18 months of age. Body weight (668 vs. 764 kg, <I>P</I> = 0.011), body weight gain (1 223 vs. 1 385 g/day, <I>P</I> = 0.043), and body protein gain (93 vs. 128 g/day, <I>P</I> = 0.001) were lower in H compared to CH bulls. Protein expense per kg protein accretion was higher in H bulls (13.8 vs. 10.2, <I>P</I> = 0.001). No significant differences were found in concentration and pattern of ruminal short chain fatty acid and in apparent digestibility of organic matter, crude fibre, and N-free extracts. There were no significant differencs in all morphometric traits of rumen mucosa between both cattle breeds. Compared to H, the villi of CH bulls were higher in duodenum (586 vs. 495 &mu;m, <I>P</I> = 0.001) and proximal jejunum (598 vs. 518&mu;m, <I>P</I> < 0.001), the crypt were deeper in duodenum (295 vs. 358, <I>P</I>< 0.001) and proximal jejunum (292 vs. 344 &mu;m, <I>P</I> = 0.020). In contrast, the villi in ileum were higher in H (522 vs. 471 &mu;m, <I>P</I> = 0.006). The weight of total small intestine, as percentage of total body weight, was 1.1 in H and 0.8 in CH (<I>P</I> = 0.002). The utilization of food crude protein was positively related to the duodenal (<I>P</I> = 0.001) and proximal jejunal villus height (<I>P</I> = 0.003) and to the duodenal crypt depth (<I>P</I> < 0.001) and negatively related to weight of small intestine (<I>P</I> = 0.004). It is concluded, that the higher growth potential and feed efficiency in CH bulls compared to H bulls is not caused by differences in digestion processes, but in size of small intestine, and morphology of small intestinal mucosa. Obviously the duodenum and proximal jejunum of CH bulls adapt to increase the absorptive surface due to the increase in nutrient demand.

scholarly journals Exogenous leptin controls the development of the small intestine in neonatal piglets

2003 ◽  
Vol 177 (2) ◽  
pp. 215-222 ◽  
Author(s):  
J Wolinski ◽  
M Biernat ◽  
P Guilloteau ◽  
BR Westrom ◽  
R Zabielski
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Small Intestine ◽  
Intestinal Mucosa ◽  
Brush Border ◽  
Milk Formula ◽  
Small Intestinal Mucosa ◽  
Neonatal Piglets ◽  
Small Intestinal ◽  
Marker Molecule

Leptin, a hormone produced and secreted by adipose tIssue, muscles and stomach, is involved in the regulation of adipose tIssue mass, food intake and body weight in neonatal animals. It is also produced in the mammary glands and secreted into the colostrum and milk. Since leptin receptors are widely distributed in the small intestine mucosa, the aim of the present study was to investigate the effect of exogenous leptin on the development of the small intestine in neonatal piglets. Male neonatal piglets were fed with sow's milk or artificial milk formula. Every 8 h the latter received either vehicle or leptin (2 or 10 microg/kg body weight). The animals were either killed after 6 days of treatment and the small intestine sampled for histology and brush border enzyme activities or were tested for marker molecule (Na-fluorescein and BSA) absorption in vivo. Feeding milk formula slowed the maturation of small intestinal mucosa compared with feeding sow's milk. However, after leptin treatment the length of the small intestine was increased, and intestinal villi length, but not crypt size, was reduced compared with controls. The mitotic index was increased and the percentage of vacuolated enterocytes was reduced in the entire small intestine. Enterocyte brush border protease and lactase activities were reduced in the jejunum. Na-fluorescein marker molecule absorption did not change but that of BSA was reduced 3.8-fold. In conclusion, exogenous leptin administered in physiological doses reversed the maturation of the small intestinal mucosa to the range found in sow-reared piglets.

scholarly journals Influence of ethanol on the activity of glycosidases in rats exposed to cadmium (Cd2+).

1995 ◽  
Vol 42 (3) ◽  
pp. 297-299
Author(s):  
L P Arciuch ◽  
A Omasta ◽  
K Rostkowska ◽  
M Gałazyn-Sidorczuk ◽  
J Moniuszko-Jakoniuk ◽  
...  
Keyword(s):  
Small Intestine ◽  
Intestinal Mucosa ◽  
Small Intestinal Mucosa ◽  
Distinct Effect ◽  
Small Intestinal ◽  
Beta Galactosidase

Inhibition by ethanol of the activities of lysosomal exoglycosidases in stomach, small intestine, liver and brain of rats exposed to cadmium (Cd2+) was determined. Out of the glycosidases tested the most distinct effect of Cd2+ and ethanol administered to the rats in vivo was observed in the small intestinal mucosa in a decreasing order: N-acetyl-beta-hexosaminidase, beta-galactosidase and alpha-fucosidase.

scholarly journals Lentinan Attenuates Damage of the Small Intestinal Mucosa, Liver, and Lung in Mice with Gut-Origin Sepsis

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Zhongshen Kuang ◽  
Tingting Jin ◽  
ChangYi Wu ◽  
Yanan Zong ◽  
Panpan Yin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Small Intestine ◽  
Liver Function ◽  
Signaling Pathway ◽  
Intestinal Mucosa ◽  
Bacterial Translocation ◽  
Sham Operation ◽  
Small Intestinal Mucosa ◽  
Stress Injury ◽  
Small Intestinal

This study is aimed at exploring the effects of lentinan on small intestinal mucosa as well as lung and liver injury in mice with gut-origin sepsis. Cecal ligation and perforation (CLP) were used to construct a mouse model of gut-origin sepsis. The mice were randomly divided into six groups: sham operation group (sham), gut-origin sepsis model group (CLP), ulinastatin-positive drug control group (UTI), lentinan low concentration group (LTN-L, 5 mg/kg), lentinan medium concentration group (LTN-M, 10 mg/kg), and lentinan high concentration group (LTN-H, 20 mg/kg). H&E staining was used to detect the pathological damage of the small intestine, liver, and lung. The serum of mice in each group was collected to detect the expression changes of inflammatory cytokines, oxidative stress biomarkers, and liver function indexes. In vitro assessment of bacterial translocation was achieved through inoculated culture media. Western blot and RT-qPCR were used to detect the expression of molecules related to the NF-κB signaling pathway in the small intestine tissues of mice. The results showed that compared with the CLP group, the injury degree of the small intestine, liver, and lung in mice with gut-origin sepsis was improved with the increase of lentinan concentration. In addition, TNF-α, IL-1β, IL-6, and HMGB1 were decreased with the increase of lentinan concentration, but the expression of IL-10 was increased. Lentinan could also reduce the expression of oxidative stress injury indexes and liver function indexes and inhibit bacterial translocation to liver and lung tissues. Further mechanism investigation revealed that lentinan downregulated the expression of the NF-κB signaling pathway molecules (NF-κB, TLR4, and Bax) and upregulated the expression of occludin and Bcl-2. In conclusion, lentinan inhibits the activity of the NF-κB signaling pathway, thus attenuating injuries of small intestinal mucosa and liver and lung in mice with gut-origin sepsis and reducing the inflammatory response in the process of sepsis.

scholarly journals The bacteriology of the small intestinal mucosa of free-living reindeer

Rangifer ◽  
1994 ◽  
Vol 14 (2) ◽  
pp. 65 ◽  
Author(s):  
Wenche Sørmo ◽  
Tove H. Aagnes ◽  
Monica A. Olsen ◽  
Svein D. Mathiesen
Keyword(s):  
Intestinal Mucosa ◽  
Pyloric Sphincter ◽  
Jejunal Mucosa ◽  
Proximal Jejunum ◽  
Small Intestinal Mucosa ◽  
Free Living ◽  
Gram Positive ◽  
Bacterial Populations ◽  
Small Intestinal ◽  
Distal Jejunum

Bacteria in close associaton with the intestinal mucosa are thought to protect the mucosa from pathogenic microorganisms. The pH of the small intestinal mucosa and the viable populations of aerobic and anaerobic bacteria associated with the proximal and distal jejunal mucosa, were measured in four free-living reindeer in winter. The anaerobic bacterial populations were characterized. The median pH of the mucosa of the duodenum was 6.6 (n=4) at point 0.2 m from the pyloric sphincter. The mucosal pH increased along the length of the intestine to 8.3 at 14 m and then decreased to 7.9 at 19.8 m from the pyloric sphincter. Examination by transmission electron microscopy and cultivation techniques failed to reveal any bacteria on the mucosa of the proximal jejunum in two of the animals. In two other reindeer the median anaerobic bacterial densities in the proximal jejunum ranged from 25-2500 cells/g mucosa. The median anaerobic bacterial populations in the distal jejunum ranged from 80 to 20000 bacteria/g mucosa (n=4). The anaerobic population of bacteria in the proximal jejunum was dominated by streptococci and unidentified gram positive rods. Bacteroidaceae, streptococci and unidentified gram positive rods were common in the distal jejunum. The low density and the species diversity of bacteria in the small intestine suggests that these microorganisms are inhibited by components in the natural winter diet of reindeer. Bacteria evidently play a minor role in protection of the mucosa of reindeer in winter.

Proliferating cells in the vertebrate small intestine: an immunohistocheniical study

1995 ◽  
Vol 53 ◽  
pp. 1034-1035
Author(s):  
Làszló G. Kömüves
Keyword(s):  
Small Intestine ◽  
Intestinal Mucosa ◽  
Ambystoma Mexicanum ◽  
Nuclear Antigen ◽  
Cell Renewal ◽  
Small Intestinal Mucosa ◽  
Proliferating Cells ◽  
Citrate Buffer ◽  
Small Intestinal ◽  
Proliferating Cell

In the small intestinal mucosa of healthy adult mammals proliferating cell are confined to the crypts of Lieberkiihn. Earlier radioautographic studies identified proliferative cells in the small intestine of several non-mammalian vertebrates. However, it is still not clear whether cell renewal is confined to proliferative compartment within the small intestinal mucosa in non-mammalian vertebrates. In the present study proliferative cells were identified using an immunological marker of cell proliferation, the proliferating cell nuclear antigen (PCNA) in the small intestine of several non-mammalian vertebrate species, including birds (zebrafinch, Poephila guttata), reptiles (green anole, Anolis carolinensis), amphibia (axolotl, Ambystoma mexicanum), and fishes (goldfish, Carassius auratus).Segments of the small intestine were fixed in 4% formaldehyde in 0.86 M phosphate buffer, pH=7.2 and embedded in paraffin. Deparaffinized and rehydrated sections were microwaved in citrate buffer. The immunohistochemical detection method used in this study based on the capillary action principle, as developed by Brigati.

Cellular cross talk in the small intestinal mucosa: postnatal lymphocytic immigration elicits a specific epithelial transcriptional response

2008 ◽  
Vol 294 (6) ◽  
pp. G1335-G1343 ◽  
Author(s):  
Katrine T.-B. G. Schjoldager ◽  
Henrik R. Maltesen ◽  
Sophie Balmer ◽  
Leif R. Lund ◽  
Mogens H. Claesson ◽  
...  
Keyword(s):  
Small Intestine ◽  
Dna Microarray ◽  
Intestinal Mucosa ◽  
Cross Talk ◽  
Transcriptional Response ◽  
Pcr Analysis ◽  
Small Intestinal Mucosa ◽  
Mouse Small Intestine ◽  
Small Intestinal ◽  
Latent Structures

During the early postnatal period lymphocytes migrate into the mouse small intestine. Migrating infiltrative lymphocytes have the potential to affect the epithelial cells via secreted cytokines. Such cross talk can result in the elicitation of an epithelial transcriptional response. Knowledge about such physiological cross talk between the immune system and the epithelium in the postnatal small intestinal mucosa is lacking. We have investigated the transcriptome changes occurring in the postnatal mouse small intestine using DNA microarray technology, immunocytochemistry, and quantitative real-time RT-PCR analysis. The DNA microarray data were analyzed bioinformatically by using a combination of projections to latent structures analysis and functional annotation analysis. The results show that infiltrating lymphocytes appear in the mouse small intestine in the late postweaning period and give rise to distinct changes in the epithelial transcriptome. Of particular interest is the expression of three genes encoding a mucin ( Muc4), a mucinlike protein ( 16000D21Rik), and ATP citrate lyase (Acly). All three genes were shown to be expressed by the epithelium and to be upregulated in response to lymphocytic migration into the small intestinal mucosa.

scholarly journals The effect of glucose on the activity of phosphofructokinase in the mucosa of rat small intestine

1984 ◽  
Vol 218 (2) ◽  
pp. 459-464 ◽  
Author(s):  
A Jamal ◽  
G L Kellett ◽  
J P Robertson
Keyword(s):  
Small Intestine ◽  
Intestinal Mucosa ◽  
Small Intestinal Mucosa ◽  
Rat Small Intestine ◽  
Short Term ◽  
Small Intestinal ◽  
Rate Limiting ◽  
Effect Of Glucose ◽  
Acid Labile

In common with other phosphofructokinase isoenzymes, phosphofructokinase in the epithelial cells of rat small-intestinal mucosa is activated by fructose 2,6-bisphosphate. However, fructose 2,6-bisphosphate was found not to be present in mucosa as judged by three criteria: (1) chromatography on Sephadex G-25 of crude mucosal extracts from fed rats did not result in a decrease, or indeed any change, in the activity of phosphofructokinase under suboptimal conditions at pH7; (2) ultrafiltrates of mucosal extracts did not possess any acid-labile activating activity when tested against chromatographed liver phosphofructokinase; (3) phosphofructokinase-2 activity was not detectable in mucosal extracts. Furthermore, the perfusion in vitro of isolated loops of jejunum or the incubation of mucosal scrapings from either fed rats or rats starved for 48 h showed that the activity of mucosal phosphofructokinase is not subject to short-term regulation by glucose. These observations are consistent with the view that phosphofructokinase is the rate-limiting enzyme of glycolysis in intestinal mucosa and account for the fact that the rate of glucose utilization by rat small intestine is not very responsive to changes in the concentration of glucose in the lumen.

Effect of fasting on Na-K-ATPase activity in rat small intestinal mucosa

1980 ◽  
Vol 58 (6) ◽  
pp. 643-649 ◽  
Author(s):  
D. Murray ◽  
G. E. Wild
Keyword(s):  
Small Intestine ◽  
Atpase Activity ◽  
Intestinal Mucosa ◽  
Total Activity ◽  
Small Intestinal Mucosa ◽  
Distal Small Intestine ◽  
Adrenocortical Activity ◽  
Glucose Ingestion ◽  
Small Intestinal ◽  
Mucosal Mass

The effect of fasting on mucosal Na-K-ATPase activity in various regions of rat small intestine was investigated. Fasting (17-48 h) was associated with a consistent decrease in specific and total activity of Na-K-ATPase in the jejunum, the levels tending to rise more distally. No effect on the specific activities of Mg-ATPase or alkaline phosphatase was found. Fasting was also associated with increased adrenocortical activity and with decreases in mucosal mass, protein content, and histological dimensions of the jejunum, no similar changes being found in the distal small intestine. Glucose ingestion prevented the decrease in jejunal enzyme activity associated with fasting and elevated levels in the mid and terminal small intestine of fed animals. These effects suggest that Na-K-ATPase activity in small intestinal mucosa may be, in part, inducible.

Mucosal Peptide Hydrolase and Brush-Border Marker Enzyme Activities in Three Regions of the Small Intestine of Rats with Experimental Uraemia

1990 ◽  
Vol 79 (6) ◽  
pp. 663-668 ◽  
Author(s):  
D. J. Haines ◽  
C. H. J. Swan ◽  
J. R. B. Green ◽  
J. F. Woodley
Keyword(s):  
Enzyme Activity ◽  
Small Intestine ◽  
Intestinal Mucosa ◽  
Brush Border ◽  
Enzyme Activities ◽  
Small Intestinal Mucosa ◽  
Marker Enzyme ◽  
Small Intestinal Transit ◽  
Proximal Small Intestine ◽  
Small Intestinal

1. The activities of nine peptide hydrolases and three non-peptidase brush-border marker enzymes have been quantified in crude homogenates prepared from the proximal, mid and distal regions of small-intestinal mucosa for sham-operated (n = 9) and uraemic (n = 14) rats. Abnormalities in enzyme activities were observed in all regions studied in the uraemic group, although no reduction in food intake occurred. 2. The proximal region of the small intestine from uraemic rats showed a general fall in enzyme activities associated with the brush-border. This fall was combined with a decline in mucosal protein content. In contrast, the mid and distal regions showed increased activity against the dipeptide tyrosyl-glycine. 3. It is proposed that the fall in brush-border enzyme activities in the proximal small intestine of uraemic rats is a response to the increased water intake associated with this, and presumably other, rat models of uraemia. The increased enzyme activity against tyrosyl-glycine found in the mid and distal regions of the small intestine of uraemic rats may be caused by an increased small-intestinal transit rate, but could be an attempt to maximize tyrosine absorption in response to decreased plasma tyrosine levels. 4. This study casts doubt on specific activities being the most useful units of enzyme activity, when measured in crude homogenates prepared from the proximal small intestine of uraemic rats. It also demonstrates that enzyme activities measured at a single site in the small intestine of uraemic rats may not be representative of the enzymatic changes occurring in the small-intestinal mucosa as a whole.

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