Effects of oral supplementation with glutamate or combination of glutamate and N-carbamylglutamate on intestinal mucosa morphology and epithelium cell proliferation in weanling piglets1

2012 ◽  
Vol 90 (suppl_4) ◽  
pp. 337-339 ◽  
Author(s):  
X. Wu ◽  
Y. Zhang ◽  
Z. Liu ◽  
T. J. Li ◽  
Y. L. Yin
Keyword(s):  
Cell Proliferation ◽  
Intestinal Mucosa ◽  
Oral Supplementation ◽  
Epithelium Cell

Effects of epidermal growth factor on diamine oxidase expression and cell growth in Caco-2 cells

1991 ◽  
Vol 261 (4) ◽  
pp. G669-G676 ◽  
Author(s):  
B. Daniele ◽  
A. Quaroni
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Intestinal Mucosa ◽  
Diamine Oxidase ◽  
Small Intestinal Mucosa ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Epidermal Growth

To investigate the role of diamine oxidase (DAO) in the intestinal mucosa, we compared its expression with cell proliferation and differentiation in the human colon carcinoma cell line Caco-2. DAO synthesis was evaluated in subconfluent and confluent cultures and in the presence of epidermal growth factor (EGF), a polypeptide hormone known to have specific trophic effects on the small intestinal mucosa. EGF stimulated DNA synthesis, significantly increased cellular DAO activity and the amount of enzyme secreted into the culture medium, but decreased expression of dipeptidyl peptidase IV, a marker of cell differentiation in confluent Caco-2 cells. Immunoprecipitation of DAO from cells labeled metabolically with [35S]methionine failed to demonstrate an increased enzyme synthesis in EGF-treated cells, suggesting that this hormone acted primarily at a posttranslational level by reducing DAO degradation before intracellular storage or secretion. A possible relationship between changes in cellular DAO activity and cell proliferation was also investigated by using aminoguanidine, a specific and potent DAO inhibitor. Although DAO activity was markedly suppressed, aminoguanidine had no significant effects on the rate of DNA synthesis. These results demonstrated that in Caco-2 cells EGF stimulated DNA synthesis and DAO expression; however, cell proliferation and differentiation were not correlated with the levels of cellular DAO, suggesting that this enzyme does not play a major role in the regulation of intestinal epithelial cell turnover.

scholarly journals The transcription factor FoxM1 activates Nurr1 to promote intestinal regeneration after ischemia/reperfusion injury

2019 ◽  
Vol 51 (11) ◽  
pp. 1-12 ◽  
Author(s):  
Guo Zu ◽  
Jing Guo ◽  
Tingting Zhou ◽  
Ningwei Che ◽  
Baiying Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Intestinal Mucosa ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Epithelial ◽  
Ki 67 ◽  
Intestinal Regeneration ◽  
Foxm1 Expression ◽  
Intestinal Ischemia Reperfusion

Abstract FoxM1 is involved in the regeneration of several organs after injury and expressed in the intestinal mucosa. The intrinsic mechanism of FoxM1 activity in the mucosa after intestinal ischemia/reperfusion (I/R) injury has not been reported. Therefore, we investigated the role of FoxM1 in mediating intestinal mucosa regeneration after I/R injury. Expression of FoxM1 and the proliferation of intestinal mucosa epithelial cells were examined in rats with intestinal I/R injury and an IEC-6 cell hypoxia/reperfusion (H/R) model. The effects of FoxM1 inhibition or activation on intestinal epithelial cell proliferation were measured. FoxM1 expression was consistent with the proliferation of intestinal epithelial cells in the intestinal mucosa after I/R injury. Inhibition of FoxM1 expression led to the downregulation of Ki-67 expression mediated by the inhibited expression of Nurr1, and FoxM1 overexpression promoted IEC-6 cell proliferation after H/R injury through activating Nurr1 expression. Furthermore, FoxM1 directly promoted the transcription of Nurr1 by directly binding the promoter of Nurr1. Further investigation showed low expression levels of FoxM1, Nurr1, and Ki-67 in the intestinal epithelium of patients with intestinal ischemic injury. FoxM1 acts as a critical regulator of intestinal regeneration after I/R injury by directly promoting the transcription of Nurr1. The FoxM1/Nurr1 signaling pathway represents a promising therapeutic target for intestinal I/R injury and related clinical diseases.

scholarly journals Effect of Changes in Dietary Net Energy Concentration on Growth Performance, Fat Deposition, Skatole Production, and Intestinal Morphology in Immunocastrated Male Pigs

2021 ◽  
Author(s):  
Nina Batorek Lukač ◽  
Marjeta Čandek-Potokar ◽  
Martin Škrlep ◽  
Valentina Kubale ◽  
Etienne Labussière
Keyword(s):  
Cell Proliferation ◽  
Growth Performance ◽  
Intestinal Mucosa ◽  
Dietary Treatment ◽  
Fat Deposition ◽  
Intestinal Morphology ◽  
Net Energy ◽  
Intermediate Cell ◽  
Ascending Colon ◽  
Indole Production

Abstract Background: Nutritional requirements of heavy immunocastrated pigs (IM) and thus the appropriate feeding strategies have not been determined. Methods: The effects of a reduced net energy (NE) diet, achieved by including up to 10% dietary fiber were studied in 41 IM pigs fed ad libitum with an extended period between immunization and slaughter (i.e. 8 weeks). Traits assessed included growth performance (before and after immunization at 112 days of age), fat deposition, intestinal skatole and indole production, intestinal morphology, and cell proliferation. Results: From 84 days of age, IM pigs were fed diets with low, medium, or high NE content (LNE, MNE, and HNE diets; with 8.5, 9.3, and 10.0 MJ NE/kg). There was no effect (P > 0.10) of feed NE concentration on average daily gain or the ratio of BW gain to NE intake in any of the periods studied. However, in the period from 143 to 170 days of age, there was a tendency for a higher NE intake (P = 0.08) in pigs fed the HNE diet along with higher (P < 0.01) backfat gain. Dietary treatment affected carcass composition as lower backfat thickness (P = 0.01) and lower area of fat over the longissimus muscle (P = 0.05) were observed in LNE and MNE pigs. In addition, higher lean meat content (P = 0.04) was observed in LNE pigs. Reducing the NE of the diet with fiber addition resulted in lower indole production in the ascending colon (P < 0.01), and higher skatole production (P < 0.01) in the cecum. Greater villi area, width, height and perimeter, crypt depth, and thickness of the intestinal mucosa in the jejunum, ileum, ascending colon, and descending colon were found for the LNE group (P < 0.01) than for the HNE group, while the MNE group was intermediate. Cell proliferation was not affected by dietary treatment (P > 0.05). Conclusion: The present results show that despite improved absorptive capacity (indicated by histomorphological changes in the intestinal mucosa), a reduction in dietary NE concentration reduces lipid deposition, without affecting performance or energy efficiency in IM pigs.

scholarly journals Effects of colostrum, feeding method and oral IGF1 on porcine uterine development

Reproduction ◽  
2018 ◽  
Vol 155 (3) ◽  
pp. 259-271 ◽  
Author(s):  
Ashley F George ◽  
Kathleen M Rahman ◽  
Dori J Miller ◽  
Anne A Wiley ◽  
Meredith E Camp ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Reproductive Tract ◽  
Uterine Wall ◽  
Female Reproductive Tract ◽  
Milk Replacer ◽  
Endometrial Cell ◽  
Feeding Method ◽  
Oral Supplementation ◽  
Expression Of Genes ◽  
Uterine Development

Nursing ensures lactocrine delivery of maternally derived, milk-borne bioactive factors to offspring, which affects postnatal development of female reproductive tract tissues. Disruption of lactocrine communication for two days from birth (postnatal day (PND) 0) by feeding milk replacer in lieu of nursing or consumption of colostrum alters porcine uterine gene expression globally by PND 2 and inhibits uterine gland genesis by PND 14. Here, objectives were to determine effects of: (1) nursing or milk replacer feeding from birth; (2) a single dose of colostrum or milk replacer and method of feeding and (3) a single feeding of colostrum or milk replacer, with or without oral supplementation of IGF1, administered at birth on aspects of porcine uterine development at 12-h postnatally. Results indicate nursing for 12 h from birth supports rapid establishment of a uterine developmental program, illustrated by patterns of endometrial cell proliferation, expression of genes associated with uterine wall development and entry into mitosis and establishment of a uterine MMP9/TIMP1 system. A single feeding of colostrum at birth increased endometrial cell proliferation at 12 h, regardless of method of feeding. Oral supplementation of IGF1 was sufficient to support endometrial cell proliferation at 12 h in replacer-fed gilts, and supplementation of colostrum with IGF1 further increased endometrial cell proliferation. Results indicate that lactocrine regulation of postnatal uterine development is initiated with the first ingestion of colostrum. Further, results suggest IGF1 may be lactocrine-active and support a 12-h bioassay, which can be used to identify uterotrophic lactocrine activity.

scholarly journals A Fiber-Rich Diet and Radiation-Induced Injury in the Murine Intestinal Mucosa

2021 ◽  
Vol 23 (1) ◽  
pp. 439
Author(s):  
Dilip Kumar Malipatlolla ◽  
Sravani Devarakonda ◽  
Piyush Patel ◽  
Fei Sjöberg ◽  
Ana Rascón ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Dietary Fiber ◽  
Intestinal Mucosa ◽  
Mucosal Damage ◽  
Cytokine Profile ◽  
Serum Cytokine ◽  
Ample Evidence ◽  
Crypt Fission ◽  
Macrophage Density ◽  
Radiation Induced

Dietary fiber is considered a strong intestinal protector, but we do not know whether dietary fiber protects against the long-lasting mucosal damage caused by ionizing radiation. To evaluate whether a fiber-rich diet can ameliorate the long-lasting pathophysiological hallmarks of the irradiated mucosa, C57BL/6J mice on a fiber-rich bioprocessed oat bran diet or a fiber-free diet received 32 Gray in four fractions to the distal colorectum using a linear accelerator and continued on the diets for one, six or 18 weeks. We quantified degenerating crypts, crypt fission, cell proliferation, crypt survival, macrophage density and bacterial infiltration. Crypt loss through crypt degeneration only occurred in the irradiated mice. Initially, it was most frequent in the fiber-deprived group but declined to levels similar to the fiber-consuming group by 18 weeks. The fiber-consuming group had a fast response to irradiation, with crypt fission for growth or healing peaking already at one week post-irradiation, while crypt fission in the fiber-deprived group peaked at six weeks. A fiber-rich diet allowed for a more intense crypt cell proliferation, but the recovery of crypts was eventually lost by 18 weeks. Bacterial infiltration was a late phenomenon, evident in the fiber-deprived animals and intensified manyfold after irradiation. Bacterial infiltration also coincided with a specific pro-inflammatory serum cytokine profile. In contrast, mice on a fiber-rich diet were completely protected from irradiation-induced bacterial infiltration and exhibited a similar serum cytokine profile as sham-irradiated mice on a fiber-rich diet. Our findings provide ample evidence that dietary fiber consumption modifies the onset, timing and intensity of radiation-induced pathophysiological processes in the intestinal mucosa. However, we need more knowledge, not least from clinical studies, before this finding can be introduced to a new and refined clinical practice.

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