Age- and tissue-specific induction of NHE3 by glucocorticoids in the rat small intestine

2000 ◽  
Vol 278 (4) ◽  
pp. C629-C637 ◽  
Author(s):  
Pawel R. Kiela ◽  
Yigit S. Guner ◽  
Hua Xu ◽  
James F. Collins ◽  
Fayez K. Ghishan
Keyword(s):  
Small Intestine ◽  
Glucocorticoid Receptor ◽  
Western Blot ◽  
Mrna Level ◽  
Rat Small Intestine ◽  
Adult Rats ◽  
Tissue Specific ◽  
Distal Small Intestine ◽  
Proximal Small Intestine ◽  
Specific Induction

Of the two known apical isoforms of the Na+/H+ exchanger (NHE) family, only the NHE3 gene is regulated by glucocorticoids. The aim of these studies was to investigate the mechanisms underlying the effects of methylprednisolone (MP) on expression of NHE3 in the proximal and distal small intestine of suckling and adult rats. Immunoblots showed that the glucocorticoid responsiveness in the proximal small intestine was greatest in suckling animals (NHE3/β-actin: 0.43 ± 0.09 control vs. 1.57 ± 0.15 MP; P < 0.001), and responsiveness decreased with age with no effect in adults (0.56 ± 0.14 vs. 0.64 ± 0.17). Distal small intestine was responsive only in adult rats (0.49 ± 0.13 vs. 1.65 ± 0.09; P < 0.001). This pattern was confirmed at the mRNA level and by 22Na+ uptake. Western blot and [3H]dexamethasone mesylate binding showed that the responsiveness of NHE3 to glucocorticoids is directly related to the expression of glucocorticoid receptor (GR) in the small intestine. These studies suggest that loss and gain of glucocorticoid responsiveness in the proximal and distal small intestine, respectively, are related to age- and segment-dependent expression of GR.

Intestinal myoelectrical activity and transit time in chronic portal hypertension

1992 ◽  
Vol 263 (4) ◽  
pp. G474-G479 ◽  
Author(s):  
J. J. Stewart ◽  
H. D. Battarbee ◽  
G. E. Farrar ◽  
K. W. Betzing
Keyword(s):  
Small Intestine ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Transit Time ◽  
Experimental Period ◽  
Phase Iii ◽  
Adult Rats ◽  
Myoelectrical Activity ◽  
Distal Small Intestine ◽  
Proximal Small Intestine

This study was designed to determine the effects of portal hypertension on intestinal myoelectrical activity and propulsion. In a single surgery, adult rats were implanted with a serosal electrode at each quarter of the small intestine, and portal hypertension was produced by calibrated constriction of the portal vein. To determine intestinal transit, portal vein-stenosed (PVS) and sham-operated animals were chronically implanted with a catheter in the proximal small intestine. Transit time was determined by measuring the progression of radioactive chromium along the bowel. Studies were conducted 6, 9, and 14 days after surgical preparation. Portal hypertension was associated with both transient and persistent changes in intestinal myoelectrical activity during the experimental period. Slow wave frequency was significantly reduced in the proximal small intestine on all test days and in the distal small intestine on day 14. Occurrence of the migrating myoelectric complex was reduced on days 6 and 9. Phase III amplitude was significantly reduced in the distal small intestine on all test days. Changes in intestinal myoelectrical activity in PVS animals were not associated with measurable changes in intestinal propulsion. The results suggest that both transient and persistent changes in intestinal myoelectrical activity occur during the 2-wk period after portal vein stenosis. The functional significance of the changes is unknown.

scholarly journals The development of arylsulphatase in the small intestine of the rat

1969 ◽  
Vol 114 (2) ◽  
pp. 343-350 ◽  
Author(s):  
S. H. Danovitch ◽  
L. Laster
Keyword(s):  
Small Intestine ◽  
Specific Activity ◽  
Sprague Dawley ◽  
Adult Rats ◽  
Ph Optimum ◽  
Distal Small Intestine ◽  
Sprague Dawley Rats ◽  
Proximal Small Intestine ◽  
Liver And Kidney ◽  
Old Rats

1. Arylsulphatase activity was measured in stomach, proximal and distal third of small intestine, colon, liver and kidney of foetal and neonatal Sprague–Dawley rats and Swiss mice, with nitrocatechol sulphate as substrate. 2. The specific activity in the distal small intestine, but not in the stomach, proximal small intestine or colon, increased about fourfold between 5 and 16 days after birth in both conventional and germ-free rats. 3. No comparable increase occurred in the distal small intestine of the mouse. 4. The specific activity of acid phosphatase in the distal small intestine of the rat rose only slightly when the arylsulphatase activity increased. 5. The pH optimum and Michaelis constant of arylsulphatase activity of the distal small intestine were similar for 1-day-old, 9-day-old and adult rats. 6. When extracts of distal small intestine of 1-day-old and 9-day-old rats were incubated together, the arylsulphatase activities were additive.

Sequence, tissue distribution, and functional characterization of the rat fructose transporter GLUT5

1993 ◽  
Vol 264 (6) ◽  
pp. G1169-G1176 ◽  
Author(s):  
E. B. Rand ◽  
A. M. Depaoli ◽  
N. O. Davidson ◽  
G. I. Bell ◽  
C. F. Burant
Keyword(s):  
Small Intestine ◽  
Functional Characterization ◽  
Cdna Probe ◽  
Amino Acid Identity ◽  
Human Testis ◽  
Cdna Clones ◽  
Rat Tissues ◽  
Rat Small Intestine ◽  
Cross Hybridization ◽  
Distal Small Intestine

cDNA clones encoding rat GLUT5-small intestinal facilitative hexose transporter were isolated from a jejunum library by cross-hybridization with a human GLUT5 cDNA probe. The cDNA sequence indicates that rat GLUT5 is composed of 502 amino acids and has 81.5% amino acid identity and 87.3% similarity with the sequence of human GLUT5. Expression of synthetic rat GLUT5 mRNA in Xenopus oocytes showed that rat GLUT5 was able to mediate the uptake of fructose and, to a lesser extent, of glucose. RNA blotting studies showed that GLUT5 mRNA was present in rat small intestine, kidney, and brain. Although GLUT5 mRNA is expressed in human testis, adipose tissue, and skeletal muscle, it could not be detected by RNA blotting in these rat tissues. Developmental studies showed low levels of GLUT5 mRNA in rat small intestine and kidney during the prenatal period with a rapid induction of GLUT5 expression occurring postnatally. In situ hybridization studies of GLUT5 mRNA expression in the small intestine revealed differential expression along the crypt-villus axis with the highest levels of mRNA being in the midvillus region. In addition, there was quantitatively more GLUT5 mRNA detected in the proximal as opposed to the distal small intestine.

Development of fatty acid esterification mechanisms in rat small intestine.

1979 ◽  
Vol 237 (5) ◽  
pp. E399 ◽  
Author(s):  
Y F Shiau ◽  
C Umstetter ◽  
K Kendall ◽  
O Koldovsky
Keyword(s):  
Small Intestine ◽  
Fatty Acid ◽  
Total Fatty Acid ◽  
Fetal Programming ◽  
Rat Small Intestine ◽  
Adult Rats ◽  
Major Pathway ◽  
Acid Esterification ◽  
Fatty Acid Esterification

Fatty acid esterification was measured in fetal jejunal and ileal isografts implanted under the kidney capsules of adult host rats and compared to the age-controlled intestine grown in situ. Studies were conducted on the 21st, 35th, 49th, and 63rd postconceptional days, corresponding to prenatal, suckling, weaning, and weaned rats. Substantial fatty acid esterification activity was found in prenatal jejunum but not in ileum. A proximal-distal gradient of fatty acid esterification was observed in all groups grown in situ, but not in isografts. The monoglyceride pathway (MG-P) accounted for about one-third of total fatty acid esterification (TFAE) in jejunum grown in situ and remained constant through the study. In the ileum, MG-P was the major esterification pathway during the first 4 postnatal weeks, but decreased progressively after weaning to become insignificant in adult rats. TFAE fell in the jejunal isografts, whereas it increased in the ileum. MG-P remained as the major pathway in the implanted jejunum and ileum. Our studies suggest that luminal contents are probably the most important modulator for the development and maintenance of intestinal fatty acid esterification, and "fetal programming" manifested by changes in fatty acid esterification mechanisms in the isografts is less important.

Transport of butyric acid in vascularly perfused anuran small intestine: importance of pH and anion transport

1986 ◽  
Vol 250 (4) ◽  
pp. G469-G474
Author(s):  
D. Hollander ◽  
E. M. Gerard ◽  
C. A. Boyd
Keyword(s):  
Small Intestine ◽  
Butyric Acid ◽  
Nonlinear Function ◽  
Anion Transport ◽  
Transport Protein ◽  
Disulfonic Acid ◽  
Flux Analysis ◽  
Acid Transport ◽  
Distal Small Intestine ◽  
Proximal Small Intestine

Butyric acid transport was studied in the isolated, vascularly perfused frog small intestine. At luminal butyric acid concentrations of 5-50 mM, absorption was a nonlinear function of the luminal concentration, whereas the relationship of absorption to concentration remained linear at 0-1,000 microM. The most important factor regulating the rate and direction of butyric acid transport was the pH. We used unidirectional flux analysis to determine net transport across the epithelium while the pH of the luminal or vascular compartments was changed. We found a four- to fivefold decrease in butyric acid transport into the portal circulation as the lumen pH was increased from 6.0 to 8.0. The pH of the vascular perfusate influenced the vascular-to-lumen transport of butyric acid in the same proportions. The second important regulatory factor of butyric acid transport was the 4,4'-diisothiocyananostilbene-2,2'-disulfonic acid (DIDS)-sensitive anion transport protein. DIDS added to the lumen at 10(-6) M decreased butyric acid transport by approximately 40% at pH 7.4. DIDS also inhibited butyric acid transport when added to the vascular perfusate or when transport was measured in a vascular-to-lumen direction. We suggest that, at the relatively low pH of the proximal small intestine, butyric acid becomes protonated and lipophilic and is mainly transported directly through the cell membrane. At the more alkaline pH of the distal small intestine butyric acid is in the ionized form and transport by the DIDS-sensitive anion transport protein may predominate.

Pancreaticobiliary factors in the modulation of small intestinal enterokinase in the rat

1986 ◽  
Vol 250 (1) ◽  
pp. G103-G108 ◽  
Author(s):  
B. M. Newman ◽  
P. C. Lee ◽  
H. Tajiri ◽  
D. R. Cooney ◽  
E. Lebenthal
Keyword(s):  
Small Intestine ◽  
Bile Acids ◽  
Common Duct ◽  
Complete Loss ◽  
Adult Rats ◽  
Brush Border Enzymes ◽  
Proximal Small Intestine ◽  
Trophic Changes ◽  
The Common ◽  
Small Intestinal

Chronic pancreaticobiliary diversion was employed to study the modulation of enterokinase in the small intestine of adult rats. Diversion resulted in apparent trophic changes of the proximal bypassed portion of the intestinal mucosa. An almost complete loss of mucosal enterokinase activity in the proximal duodenum but no increase of enterokinase in the segments distal to reentry of the common duct was found in the pancreaticobiliary-diverted rats. The effect on the enterokinase activity in the proximal segment was specific in that no other brush-border enzymes measured in that segment were decreased. The decrease in enterokinase was partially prevented by dietary supplementation with pancreatic trypsinogen and completely avoided with the addition of a combination of bile acids and trypsinogen. Supplementation with bile acid alone did not preserve the enterokinase levels in the bypassed rats. The results suggested that trypsinogen is the primary factor responsible for modulating enterokinase levels in the proximal small intestine, with bile acids acting as a modifier.

Postnatal development of circadian rhythms in disaccharidase activities in rat small intestine.

1978 ◽  
Vol 234 (5) ◽  
pp. E500
Author(s):  
M Saito ◽  
M Suda ◽  
H Matzuda
Keyword(s):  
Small Intestine ◽  
Circadian Rhythm ◽  
Circadian Rhythms ◽  
Postnatal Development ◽  
Feeding Time ◽  
Rat Small Intestine ◽  
Suckling Period ◽  
Adult Rats ◽  
Circadian Change ◽  
Ad Libitum

The circadian rhythms in the activities of maltase and lactase of the small intestine were examined at various stages of postnatal development in rats. When the rats were fed ad libitum, no circadian change in the enzyme activities was found during the suckling period or the weaning period. However, several days after the time of weaning, the enzymes showed the same circadian changes as in adult rats with higher activities at night. After weaning, when the rats were fed only during the daytime, the phase of the enzyme rhythm shifted about half a day, and the highest activity was observed around feeding time. However, during the suckling period, no circadian rhythm in the enzyme acvities was found, even when the rats were allowed to feed only during a restricted time of the day.

scholarly journals Early changes in tissue amino acid metabolism and nutrient routing in rats fed a high-fat diet: evidence from natural isotope abundances of nitrogen and carbon in tissue proteins

2018 ◽  
Vol 119 (9) ◽  
pp. 981-991 ◽  
Author(s):  
Olivier L. Mantha ◽  
Sergio Polakof ◽  
Jean-François Huneau ◽  
François Mariotti ◽  
Nathalie Poupin ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Adipose Tissue ◽  
Small Intestine ◽  
Amino Acid ◽  
Tibialis Anterior ◽  
High Fat ◽  
Adult Rats ◽  
Peripheral Tissues ◽  
Tissue Specific ◽  
Specific Effects

AbstractLittle is known about how diet-induced obesity and insulin resistance affect protein and amino acid (AA) metabolism in tissues. The natural relative abundances of the heavy stable isotopes of C (δ13C) and N (δ15N) in tissue proteins offer novel and promising biomarkers of AA metabolism. They, respectively, reflect the use of dietary macronutrients for tissue AA synthesis and the relative metabolic use of tissue AA for oxidation v. protein synthesis. In this study, δ13C and δ15N were measured in the proteins of various tissues in young adult rats exposed perinatally and/or fed after weaning with a normal- or a high-fat (HF) diet, the aim being to characterise HF-induced tissue-specific changes in AA metabolism. HF feeding was shown to increase the routing of dietary fat to all tissue proteins via non-indispensable AA synthesis, but did not affect AA allocation between catabolic and anabolic processes in most tissues. However, the proportion of AA directed towards oxidation rather than protein synthesis was increased in the small intestine and decreased in the tibialis anterior muscle and adipose tissue. In adipose tissue, the AA reallocation was observed in the case of perinatal or post-weaning exposure to HF, whereas in the small intestine and tibialis anterior muscle the AA reallocation was only observed after HF exposure that covered both the perinatal and post-weaning periods. In conclusion, HF exposure induced an early reorganisation of AA metabolism involving tissue-specific effects, and in particular a decrease in the relative allocation of AA to oxidation in several peripheral tissues.

Role of 5-HT in cholera toxin-induced mucin secretion in the rat small intestine

1996 ◽  
Vol 270 (6) ◽  
pp. G1001-G1009 ◽  
Author(s):  
B. A. Moore ◽  
K. A. Sharkey ◽  
M. Mantle
Keyword(s):  
Small Intestine ◽  
Receptor Antagonist ◽  
Cholera Toxin ◽  
Receptor Subtypes ◽  
Rat Small Intestine ◽  
Mucin Secretion ◽  
Common Pathway ◽  
Distal Small Intestine ◽  
Intestinal Segments

We examined the role of 5-hydroxytryptamine (5-HT) in cholera toxin (CT)-induced mucin secretion in the proximal and distal regions of the rat small intestine. Neither the 5-HT2 receptor antagonist ketanserin nor the cyclooxygenase inhibitor indomethacin was capable of inhibiting choleraic mucin secretion. However, in the presence of the mixed 5-HT3/4 receptor antagonist tropisetron at doses that block both receptor subtypes, the secretory response was reduced to baseline levels in the proximal and distal small intestine. The selective 5-HT3 receptor antagonist ondansetron had no significant effect. These findings suggest that choleraic mucin secretion is mediated primarily through the activation of a 5-HT4-like receptor. Mucin secretion in response to the exogenous application of 5-HT occurs via two pathways: one is mediated by a 5-HT4-like receptor and is capsaicin sensitive but tetrodotoxin (TTX) insensitive, and one lacks the capsaicin-sensitive 5-HT4-mediated response but is TTX sensitive. Both converge on a common pathway that is cholinergic. No significant differences were observed between proximal and distal intestinal segments.

Variation in Rotavirus Virulence: A Comparison of Pathogenesis in Calves between Two Rotaviruses of Different Virulence

1993 ◽  
Vol 30 (3) ◽  
pp. 223-233 ◽  
Author(s):  
G. A. Hall ◽  
J. C. Bridger ◽  
K. R. Parsons ◽  
R. Cook
Keyword(s):  
Small Intestine ◽  
Virulent Strain ◽  
Villus Height ◽  
Distal Small Intestine ◽  
Cytopathic Effects ◽  
Proximal Small Intestine ◽  
Viral Particles ◽  
Virulent Virus ◽  
The Mean ◽  
Spread Of Infection

Variation in virulence between two bovine rotaviruses was investigated using ten female and ten male 10-day-old gnotobiotic calves of five breeds or cross breeds that were inoculated with a virulent strain or a strain of low virulence. Similar numbers of infectious viral particles were detected in feces of calves inoculated with either virus, but diarrhea, xylose malabsorption, and reduction of villus height occurred only after inoculation with virulent virus. The mean percentage of the area of the villus epithelium per villus immunostained for rotavirus antigen was eight times greater in calves inoculated with virulent virus, and the mean percentage of villi on which immunostained enterocytes were detected was twice as large in calves inoculated with virulent virus than in calves inoculated with the virus of low virulence. Mean crypt death and mean crypt cell production rates were increased after inoculation with either virus. Virulence was associated with extensive spread of infection through the small intestine, preferential colonization of the proximal small intestine, and marked damage to enterocytes and villi. The virus of low virulence infected the proximal small intestine poorly, and although it infected more enterocytes in the mid and distal small intestine and replicated in them, causing cytopathic effects, it did not damage intestinal structure and affect function.

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