Luminal fructose modulates fructose transport and GLUT-5 expression in small intestine of weaning rats

1998 ◽  
Vol 274 (2) ◽  
pp. G232-G239 ◽  
Author(s):  
Rong Shu ◽  
Elmer S. David ◽  
Ronaldo P. Ferraris
Keyword(s):  
Brush Border ◽  
Intestinal Lumen ◽  
Mrna Levels ◽  
Neonatal Rats ◽  
Early Weaning ◽  
Feeding Duration ◽  
High Fructose ◽  
Uptake Rates ◽  
Dietary Fructose ◽  
Baseline Levels

In neonatal rats, precocious introduction of dietary fructose significantly enhances brush-border fructose transport rates and GLUT-5 mRNA levels during early weaning. In this study, these rates and levels were more than two times higher in the anastomosed intestine compared with those in the bypassed loop of weaning pups that underwent Thiry-Vella surgery and consumed high-fructose (HF) diets. In Thiry-Vella pups fed fructose-free (NF) diets, uptake rates and mRNA levels in the anastomosed intestine were very low and similar to those in the bypassed loop. In sham-operated littermates, transport rates and mRNA levels were similar between intestinal regions that corresponded to anastomosed and bypassed loops in Thiry-Vella pups and were two to three times greater in pups fed HF than in those fed NF diet. In contrast, rates of brush-border glucose transport and levels of SGLT-1 and of GLUT-2 mRNA were independent of diet and were similar between bypassed and anastomosed regions. Changes in GLUT-5 expression did not follow a distinct diurnal rhythm. When pups were fed HF diet after 12 h of starvation to empty the intestinal lumen, fructose transport rates increased with feeding duration and reached a plateau 12–24 h after feeding; in contrast, GLUT-5 mRNA levels were highest within 4 h after arrival of chyme in the jejunum and then decreased gradually and returned to baseline levels 24 h later. In littermates fed NF diet, mRNA levels and uptake rates were each independent of feeding duration. Luminal, and not endocrine, signals regulate GLUT-5 expression in weaning pups.

Dietary fructose enhances intestinal fructose transport and GLUT5 expression in weaning rats

1997 ◽  
Vol 272 (3) ◽  
pp. G446-G453 ◽  
Author(s):  
R. Shu ◽  
E. S. David ◽  
R. P. Ferraris
Keyword(s):  
Glucose Uptake ◽  
Brush Border ◽  
Nutrient Transport ◽  
Neonatal Rats ◽  
Ontogenetic Changes ◽  
Sucrase Activity ◽  
Uptake Rates ◽  
Dietary Fructose ◽  
Enhanced Expression ◽  
Low Levels

Rates of fructose uptake by the small intestine of neonatal rats are typically very low from parturition through weaning but undergo a dramatic increase immediately after weaning is completed. In this study, we used intestinal fructose transport as a model to determine whether nutrient transport, normally enhanced only after completion of weaning, can be enhanced earlier during development. We found that ontogenetic changes in levels of GLUT5 mRNA correlate well with already known ontogenetic changes in rates of intestinal fructose transport: low levels and rates during suckling and weaning, and high levels and rates after weaning. In contrast, levels of GLUT2 and SGLT1 mRNA were relatively more elevated throughout the suckling and weaning periods. We then found that increased expression of GLUT5 mRNA caused by dietary fructose or sucrose paralleled diet-dependent increases in brush-border fructose uptake. Rates of brush-border glucose uptake and levels of SGLT1 and GLUT2 mRNA were not enhanced by dietary fructose, glucose, or sucrose. Finally, we found that rates of fructose uptake, levels of GLUT5 mRNA, and specific sucrase activity each increased with increasing concentrations of dietary fructose given precociously to midweaning rats. In contrast, brush-border glucose uptake was independent of dietary fructose concentration. Thus precocious introduction of dietary fructose causes enhanced expression of fructose transporters earlier during development. This effect is specific: only luminal fructose is effective, and only brush-border fructose transport can be modulated. These results unveil the potential for regulating nutrient transport early in development.

GLUT-5 expression in neonatal rats: crypt-villus location and age-dependent regulation

2001 ◽  
Vol 281 (3) ◽  
pp. G666-G674 ◽  
Author(s):  
Lan Jiang ◽  
Elmer S. David ◽  
Noel Espina ◽  
Ronaldo P. Ferraris
Keyword(s):  
Mrna Expression ◽  
High Glucose ◽  
Mrna Abundance ◽  
Neonatal Rats ◽  
Age Dependence ◽  
Early Feeding ◽  
High Fructose ◽  
Uptake Rates ◽  
Age Dependent

The rat fructose transporter normally appears after completion of weaning but can be precociously induced by early feeding of a high-fructose diet. In this study, the crypt-villus site, the metabolic nature of the signal, and the age dependence of induction were determined. In weaning rats fed high-glucose pellets, GLUT-5 mRNA expression was modest, localized mainly in the upper three-fourths of the villus, and there was little expression in the villus base. When fed high-fructose pellets, GLUT-5 mRNA expression was two to three times greater in all regions except the villus base. Intestinal perfusion in vivo of a nonmetabolizable fructose analog, 3- O-methylfructose, tended to increase fructose uptake rate and moderately increased GLUT-5 mRNA abundance but had no effect on glucose uptake rates and SGLT1 mRNA abundance. Gavage feeding of high-fructose, but not high-glucose, solutions enhanced fructose uptake only in pups ≥14 days, suggesting that GLUT-5 regulation is markedly age dependent. Fructose or its metabolites upregulate GLUT-5 expression in all enterocytes, except those in the crypt and villus base and in pups <14 days old.

scholarly journals High-fructose corn syrup enhances intestinal tumor growth in mice

Science ◽  
2019 ◽  
Vol 363 (6433) ◽  
pp. 1345-1349 ◽  
Author(s):  
Marcus D. Goncalves ◽  
Changyuan Lu ◽  
Jordan Tutnauer ◽  
Travis E. Hartman ◽  
Seo-Kyoung Hwang ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Tumor Grade ◽  
Intestinal Lumen ◽  
High Fructose Corn Syrup ◽  
Moderate Dose ◽  
Corn Syrup ◽  
High Fructose ◽  
Increased Risk ◽  
Excessive Consumption ◽  
Support Tumor Growth

Excessive consumption of beverages sweetened with high-fructose corn syrup (HFCS) is associated with obesity and with an increased risk of colorectal cancer. Whether HFCS contributes directly to tumorigenesis is unclear. We investigated the effects of daily oral administration of HFCS in adenomatous polyposis coli (APC) mutant mice, which are predisposed to develop intestinal tumors. The HFCS-treated mice showed a substantial increase in tumor size and tumor grade in the absence of obesity and metabolic syndrome. HFCS increased the concentrations of fructose and glucose in the intestinal lumen and serum, respectively, and the tumors transported both sugars. Within the tumors, fructose was converted to fructose-1-phosphate, leading to activation of glycolysis and increased synthesis of fatty acids that support tumor growth. These mouse studies support the hypothesis that the combination of dietary glucose and fructose, even at a moderate dose, can enhance tumorigenesis.

Transepithelial transport of cholyltaurine by Caco-2 cell monolayers is sodium dependent

1993 ◽  
Vol 264 (6) ◽  
pp. G1118-G1125 ◽  
Author(s):  
C. E. Chandler ◽  
L. M. Zaccaro ◽  
J. B. Moberly
Keyword(s):  
Bile Acids ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Incubation Temperature ◽  
Membrane Vesicles ◽  
Metabolic Inhibitors ◽  
Intestinal Lumen ◽  
Transepithelial Transport ◽  
Reverse Direction ◽  
Dependent Transport

Bile acids are efficiently recovered from the intestinal lumen by a Na(+)-dependent transport process that is localized in the ileal enterocyte brush-border membrane. To establish a cell culture model for this process, we examined the Na+ dependence of cholyltaurine (C-tau; taurocholate) transport across monolayers of differentiated Caco-2 cells grown on permeable filter inserts. Transport of [3H]C-tau was Na+ dependent (> 20-fold stimulation), saturable, and time linear for at least 60 min. The apparent Michaelis constant of [3H]C-tau transport was approximately 65 microM, and the maximal transport rate was approximately 800 pmol.min-1.mg protein-1. Transport of [3H]C-tau in the apical-to-basolateral direction was 17-fold greater than transport in the reverse direction. Lowered incubation temperature, various metabolic inhibitors, and various unlabeled bile acids inhibited [3H]C-tau transport. Caco-2 cells thus transport bile acids in a manner similar to that described for ileal brush-border membrane vesicles and isolated ileal enterocytes and are therefore an appropriate model for studying the molecular basis of ileal bile acid transport.

Pattern of rat intestinal brush-border enzyme gene expression changes with epithelial growth state

1995 ◽  
Vol 269 (2) ◽  
pp. C385-C391 ◽  
Author(s):  
R. A. Hodin ◽  
S. M. Chamberlain ◽  
S. Meng
Keyword(s):  
Gene Expression ◽  
Alkaline Phosphatase ◽  
Brush Border ◽  
Longitudinal Axis ◽  
Mrna Levels ◽  
Intestinal Alkaline Phosphatase ◽  
Enzyme Gene ◽  
Growth State ◽  
Brush Border Enzyme ◽  
Epithelial Growth

Enterocyte growth and differentiation occur simultaneously within the epithelium, but little is known regarding any relationship between these two processes. Four rat models of small intestinal epithelial hypo- and hyperplasia (neonatal ontogeny, fasting/refeeding, hypo-/hyperthyroidism, and bombesin treatment) were used to study the regulation of enterocyte gene expression in relation to epithelial growth state. Mucosal scrapings, as well as crypt and villus cell populations, were subjected to Northern blot analyses using radiolabeled cDNA probes corresponding to lactase, intestinal alkaline phosphatase, villin, ornithine decarboxylase (ODC), and the actin control. In all four models, the hypoplastic (atrophic) condition is characterized by high levels of lactase and low levels of the 3.0-kb intestinal alkaline phosphatase mRNA, whereas under hyperplastic conditions this pattern is reversed. The changes in intestinal alkaline phosphatase and lactase are qualitatively similar along the longitudinal axis of the intestine and are proportional to the degree of hyperplasia, as verified by ODC mRNA levels. Furthermore, the crypt-villus axis of differentiation is maintained regardless of epithelial growth state. In conclusion, the pattern of brush-border enzyme gene expression changes as a function of epithelial growth state, indicating a previously unrecognized degree of plasticity to the state of enterocyte differentiation.

Development of gonadal feedback regulation of gonadotropin gene expression and secretion in female rats

1992 ◽  
Vol 127 (5) ◽  
pp. 454-458 ◽  
Author(s):  
Pirjo A Pakarinen ◽  
Ilpo T Huhtaniemi
Keyword(s):  
Negative Feedback ◽  
Feedback Regulation ◽  
Female Rats ◽  
Mrna Levels ◽  
Neonatal Rats ◽  
Adult Rats ◽  
Gonadotropin Secretion ◽  
Negative Feedback Regulation ◽  
Pituitary Gonadotropin ◽  
Old Adult

The postnatal development of the gonadal negative feedback control of gonadotropins was studied in female rats. Neonatal (5-day-old) and randomly cycling young (60-day-old) and more mature (180-day-old) adult rats were ovariectomized, and half of them received Silastic implants containing the synthetic estrogen, diethylstilbestrol. The neonatal rats were killed 5, 10 or 15 days, and the adult rats 7 days after the operation. Age-matched and sham-operated animals served as controls. There were no statistically significant responses of serum LH or FSH concentrations or of the pituitary gonadotropin subunit mRNA levels to ovariectomy at any of the neonatal ages. A marked increase (p<0.01) after ovariectomy was seen in serum gonadotropins and in the cognate mRNA levels at both adult ages. In spite of the weak feedback response of the neonatal rats to ovariectomy, diethylstilbestrol suppressed the basal pituitary gonadotropin concentrations and the specific LH and FSH β-chain mRNAs (p<0.01–0.05). These results demonstrate that the gonadal negative feedback regulation of gonadotropin synthesis and secretion is not fully developed in neonatal and prepubertal female rats before 20 days of age. This is probably due to the steroidogenic quiescence of the ovaries in early life. However, the capability of the pituitary to respond to negative estrogen feedback has developed in the neonatal female, as demonstrated by the suppressive effects of diethylstilbestrol treatment on gonadotropin secretion.

scholarly journals The enterocyte microvillus is a vesicle-generating organelle

2009 ◽  
Vol 185 (7) ◽  
pp. 1285-1298 ◽  
Author(s):  
Russell E. McConnell ◽  
James N. Higginbotham ◽  
David A. Shifrin ◽  
David L. Tabb ◽  
Robert J. Coffey ◽  
...  
Keyword(s):  
Brush Border ◽  
Membrane Surface ◽  
Intestinal Lumen ◽  
Intestinal Alkaline Phosphatase ◽  
Brush Border Enzymes ◽  
Membrane Surface Area ◽  
Catalytically Active ◽  
The Right

For decades, enterocyte brush border microvilli have been viewed as passive cytoskeletal scaffolds that serve to increase apical membrane surface area. However, recent studies revealed that in the in vitro context of isolated brush borders, myosin-1a (myo1a) powers the sliding of microvillar membrane along core actin bundles. This activity also leads to the shedding of small vesicles from microvillar tips, suggesting that microvilli may function as vesicle-generating organelles in vivo. In this study, we present data in support of this hypothesis, showing that enterocyte microvilli release unilamellar vesicles into the intestinal lumen; these vesicles retain the right side out orientation of microvillar membrane, contain catalytically active brush border enzymes, and are specifically enriched in intestinal alkaline phosphatase. Moreover, myo1a knockout mice demonstrate striking perturbations in vesicle production, clearly implicating this motor in the in vivo regulation of this novel activity. In combination, these data show that microvilli function as vesicle-generating organelles, which enable enterocytes to deploy catalytic activities into the intestinal lumen.

scholarly journals The effect of human amnion epithelial cells on lung development and inflammation in preterm lambs exposed to antenatal inflammation

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0253456
Author(s):  
Paris Clarice Papagianis ◽  
Siavash Ahmadi-Noorbakhsh ◽  
Rebecca Lim ◽  
Euan Wallace ◽  
Graeme Polglase ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Epithelial Cells ◽  
Lung Development ◽  
Lung Inflammation ◽  
Respiratory Support ◽  
Mrna Levels ◽  
Weaning From Mechanical Ventilation ◽  
Early Weaning ◽  
Human Amnion ◽  
Amnion Epithelial Cells

Background Lung inflammation and impaired alveolarization are hallmarks of bronchopulmonary dysplasia (BPD). We hypothesize that human amnion epithelial cells (hAECs) are anti-inflammatory and reduce lung injury in preterm lambs born after antenatal exposure to inflammation. Methods Pregnant ewes received either intra-amniotic lipopolysaccharide (LPS, from E.coli 055:B5; 4mg) or saline (Sal) on day 126 of gestation. Lambs were delivered by cesarean section at 128 d gestation (term ~150 d). Lambs received intravenous hAECs (LPS/hAECs: n = 7; 30x106 cells) or equivalent volumes of saline (LPS/Sal, n = 10; or Sal/Sal, n = 9) immediately after birth. Respiratory support was gradually de-escalated, aimed at early weaning from mechanical ventilation towards unassisted respiration. Lung tissue was collected 1 week after birth. Lung morphology was assessed and mRNA levels for inflammatory mediators were measured. Results Respiratory support required by LPS/hAEC lambs was not different to Sal/Sal or LPS/Sal lambs. Lung tissue:airspace ratio was lower in the LPS/Sal compared to Sal/Sal lambs (P<0.05), but not LPS/hAEC lambs. LPS/hAEC lambs tended to have increased septation in their lungs versus LPS/Sal (P = 0.08). Expression of inflammatory cytokines was highest in LPS/hAECs lambs. Conclusions Postnatal administration of a single dose of hAECs stimulates a pulmonary immune response without changing ventilator requirements in preterm lambs born after intrauterine inflammation.

Hormonal and environmental regulation of epithelial calcium channel in gill of rainbow trout (Oncorhynchus mykiss)

2006 ◽  
Vol 291 (5) ◽  
pp. R1490-R1498 ◽  
Author(s):  
Arash Shahsavarani ◽  
Steve F. Perry
Keyword(s):  
Protein Expression ◽  
Fold Increase ◽  
Mrna Levels ◽  
Uptake Capacity ◽  
Pavement Cells ◽  
Protein Levels ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Uptake Rates ◽  
Mrna And Protein Expression ◽  
Trout Gill

We indirectly tested the idea that the epithelial Ca2+ channel (ECaC) of the trout gill is regulated in an appropriate manner to adjust rates of Ca2+ uptake. This was accomplished by assessing the levels of gill ECaC mRNA and protein in fish exposed to treatments known to increase or decrease Ca2+ uptake capacity. Exposure of trout to soft water ([Ca2+] = 20–30 nmol/l) for 5 days (a treatment known to increase Ca2+ uptake capacity) caused a significant increase in ECaC mRNA levels and an increase in ECaC protein expression. The inducement of hypercalcemia by infusing fish with CaCl2 (a treatment known to reduce Ca2+ uptake) was associated with a significant decrease in ECaC mRNA levels, yet protein levels were unaltered. ECaC mRNA and protein expression were increased in fish treated with the hypercalcemic hormone cortisol. Finally, exposure of trout to 48 h of hypercapnia (∼7.5 mmHg, a treatment known to increase Ca2+ uptake capacity) elicited an ∼100-fold increase in the levels of ECaC mRNA and a significant increase in protein expression. Immunocytochemical analysis of the gills from hypercapnic fish suggested a marked increase in the apical expression of ECaC on pavement cells and a subpopulation of mitochondria-rich cells. The results of this study provide evidence that Ca2+ uptake rates are, in part, regulated by the numbers of apical membrane Ca2+ channels that, in turn, modulate the inward flux of Ca2+ into gill epithelial cells.

Sign in / Sign up

Export Citation Format

Share Document