Peptide YY enhances NaCl and water absorption in the rat colon in vivo

1992 ◽  
Vol 48 (1) ◽  
pp. 47-50 ◽  
Author(s):  
M. Okuno ◽  
T. Nakanishi ◽  
Y. Shinomura ◽  
T. Kiyohara ◽  
H. Ishikawa ◽  
...  
Keyword(s):  
Water Absorption ◽  
Peptide Yy ◽  
Rat Colon

Neural mechanism of the antisecretory effect of peptide YY in the rat colon in vivo

Peptides ◽  
2000 ◽  
Vol 21 (1) ◽  
pp. 59-63 ◽  
Author(s):  
Jacques Chariot ◽  
Annick Tsocas ◽  
Abdelaziz Souli ◽  
Olivier Presset ◽  
Claude Rozé
Keyword(s):  
Peptide Yy ◽  
Neural Mechanism ◽  
Rat Colon ◽  
Antisecretory Effect

scholarly journals Na, Cl, and Water Transport by Rat Colon

1960 ◽  
Vol 43 (3) ◽  
pp. 555-571 ◽  
Author(s):  
Peter F. Curran ◽  
Gordon F. Schwartz
Keyword(s):  
Water Absorption ◽  
Water Transport ◽  
Potential Gradient ◽  
Model System ◽  
Linear Functions ◽  
Rat Colon ◽  
Na Transport ◽  
Nacl Concentration ◽  
Net Fluxes

Segments of the colon of anesthetized rats have been perfused in vivo with isotonic NaCl solutions and isotonic mixtures of NaCl and mannitol. Unidirectional and net fluxes of Na and Cl and the net fluxes of water and mannitol have been measured. Net water transport was found to depend directly on the rate of net Na transport. There was no water absorption from these isotonic solutions in the absence of net solute transport, indicating that water transport in the colon is entirely a passive process. At all NaCl concentrations studied, the lumen was found to be electrically negative to the surface of the colon by 5 to 15 mv. Na fluxes both into and out of the lumen were linear functions of NaCl concentration in the lumen. Net Na absorption from lumen to plasma has been observed to take place against an electrochemical potential gradient indicating that Na is actively transported. This active Na transport has been interpreted in terms of a carrier model system. Cl transport has been found to be due almost entirely to passive diffusion.

Study of acute pharmacologic effects of prolactin on calcium and water transport in the rat colon by an in vivo perfusion technique

2001 ◽  
Vol 79 (5) ◽  
pp. 415-421 ◽  
Author(s):  
Nateetip Krishnamra ◽  
Jiraporn Ousingsawat ◽  
Liangchai Limlomwongse
Keyword(s):  
Water Absorption ◽  
Water Transport ◽  
The Other ◽  
Rat Colon ◽  
Perfusion Technique ◽  
Perfusion Rate ◽  
Calcium Fluxes ◽  
Other Hand ◽  
Water Secretion

We investigated the acute effect of intraperitoneally administered prolactin on calcium and water transport in colon of sexually mature female Wistar rats using an in vivo perfusion technique. Test solution containing (in mM) NaCl, 100; KCl, 4.7; MgSO4, 1.2; CaCl2, 20; D-glucose, 11; sodium ferrocyanide (Na4Fe(CN)6), an index of net water transport, 20; and 0.7 (µCi 45CaCl2 (1 Ci = 37 GBq) was perfused througth the 8-cm colonic loop for 60 min at perfusion rates of 0.5 or 1.0 mL·min–1. Calcium and water transport was also studied under a no flow condition to stimulate the condition often found in the colon by in vivo ligated colonic loop for 30 min. Control results showed no correlation between calcium transport and water flux. Flow of luminal solution at 0.5 and 1.0 mL·min–1 was found to reverse net calcium absorption from 0.04 ± 0.01 nmol·g–1 dry weight·h–1 to net calcium secretion of 0.04 ± 0.04 and 0.9 ± 0.02 nmol·g–1 dry weight·h–1, respectively. Neither 0.4, 0.6, nor 1.0 mg·kg–1 prolactin had any effect on calcium fluxes in the colon. On the other hand, at a perfusion rate of 1 mL·min–1, 0.4 mg·kg–1 prolactin significantly decreased net water absorption from 3.86 ± 0.90 to 0.88 ± 0.64 mL·g–1 dry weight·h–1 (P < 0.001), and the higher doses of 0.6 and 1.0 mg·kg–1 prolactin reversed net water absorption to net water secretion of 2.20 ± 0.63 and 2.33 ± 0.89 mL·g–1 dry weight·h–1, respectively (P < 0.001). The stimulatory effect of prolactin on water transport was completely abolished by reducing the perfusion rate from 1.0 mL·min–1 to zero. The stimulatory effect of prolactin on water secretion at perfusion rate of 1.0 mL·min–1 was also abolished when luminal [Na+] was reduced from 180 to 80 mM. We concluded that, unlike in the small intestine, calcium fluxes in the colon are not related to water transport and did not respond at all to prolactin. Water transport, on the other hand, was reversed from net absorption to secretion by prolactin. We propose that this prolactin-induced water secretion is probably mediated by recycling of luminal sodium in the vicinity of tight junctions.Key words: calcium fluxes, colon, perfusion technique, prolactin, water transport.

scholarly journals Effects of Bacterial CLPB Protein Fragments on Food Intake and PYY Secretion

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2223
Author(s):  
Manon Dominique ◽  
Nicolas Lucas ◽  
Romain Legrand ◽  
Illona-Marie Bouleté ◽  
Christine Bôle-Feysot ◽  
...  
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Molecular Mimicry ◽  
Potential Effect ◽  
In Vivo Studies ◽  
Sprague Dawley ◽  
E Coli ◽  
In Vivo Effects

CLPB (Caseinolytic peptidase B) protein is a conformational mimetic of α-MSH, an anorectic hormone. Previous in vivo studies have already shown the potential effect of CLPB protein on food intake and on the production of peptide YY (PYY) by injection of E. coli wild type (WT) or E. coli ΔClpB. However, until now, no study has shown its direct effect on food intake. Furthermore, this protein can fragment naturally. Therefore, the aim of this study was (i) to evaluate the in vitro effects of CLPB fragments on PYY production; and (ii) to test the in vivo effects of a CLPB fragment sharing molecular mimicry with α-MSH (CLPB25) compared to natural fragments of the CLPB protein (CLPB96). To do that, a primary culture of intestinal mucosal cells from male Sprague–Dawley rats was incubated with proteins extracted from E. coli WT and ΔCLPB after fragmentation with trypsin or after a heat treatment of the CLPB protein. PYY secretion was measured by ELISA. CLPB fragments were analyzed by Western Blot using anti-α-MSH antibodies. In vivo effects of the CLPB protein on food intake were evaluated by intraperitoneal injections in male C57Bl/6 and ob/ob mice using the BioDAQ® system. The natural CLPB96 fragmentation increased PYY production in vitro and significantly decreased cumulative food intake from 2 h in C57Bl/6 and ob/ob mice on the contrary to CLPB25. Therefore, the anorexigenic effect of CLPB is likely the consequence of enhanced PYY secretion.

scholarly journals Bile acids drive colonic secretion of glucagon-like-peptide 1 and peptide-YY in rodents

2019 ◽  
Vol 316 (5) ◽  
pp. G574-G584 ◽  
Author(s):  
Charlotte Bayer Christiansen ◽  
Samuel Addison Jack Trammell ◽  
Nicolai Jacob Wewer Albrechtsen ◽  
Kristina Schoonjans ◽  
Reidar Albrechtsen ◽  
...  
Keyword(s):  
Bile Acids ◽  
G Protein ◽  
Peptide Yy ◽  
Whole Body ◽  
Rat Colon ◽  
G Protein Coupled Receptor ◽  
L Cells ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
G Protein Coupled

A large number of glucagon-like-peptide-1 (GLP-1)- and peptide-YY (PYY)-producing L cells are located in the colon, but little is known about their contribution to whole body metabolism. Since bile acids (BAs) increase GLP-1 and PYY release, and since BAs spill over from the ileum to the colon, we decided to investigate the ability of BAs to stimulate colonic GLP-1 and PYY secretion. Using isolated perfused rat/mouse colon as well as stimulation of the rat colon in vivo, we demonstrate that BAs significantly enhance secretion of GLP-1 and PYY from the colon with average increases of 3.5- and 2.9-fold, respectively. Furthermore, we find that responses depend on BA absorption followed by basolateral activation of the BA-receptor Takeda-G protein-coupled-receptor 5. Surprisingly, the apical sodium-dependent BA transporter, which serves to absorb conjugated BAs, was not required for colonic conjugated BA absorption or conjugated BA-induced peptide secretion. In conclusion, we demonstrate that BAs represent a major physiological stimulus for colonic L-cell secretion.NEW & NOTEWORTHY By the use of isolated perfused rodent colon preparations we show that bile acids are potent and direct promoters of colonic glucagon-like-peptide 1 and peptide-YY secretion. The study provides convincing evidence that basolateral Takeda-G protein-coupled-receptor 5 activation is mediating the effects of bile acids in the colon and thus add to the existing literature described for L cells in the ileum.

11 beta-hydroxysteroid dehydrogenase and corticosteroid hormone receptors in the rat colon

1993 ◽  
Vol 264 (6) ◽  
pp. E951-E957 ◽  
Author(s):  
C. B. Whorwood ◽  
P. C. Barber ◽  
J. Gregory ◽  
M. C. Sheppard ◽  
P. M. Stewart
Keyword(s):  
Epithelial Cells ◽  
Lamina Propria ◽  
Hormone Receptors ◽  
Rat Kidney ◽  
Distal Colon ◽  
Hydroxysteroid Dehydrogenase ◽  
Neuroendocrine Cells ◽  
Rat Colon ◽  
Mrna Levels

In the rat kidney 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) maintains normal in vivo specificity for mineralocorticoid receptor (MR) by converting the active steroid corticosterone to inactive 11-dehydrocorticosterone, leaving aldosterone to occupy the MR. Clinical observations support the hypothesis that 11 beta-HSD also protects the distal colonic MR from glucocorticoid excess. We have measured 11 beta-HSD mRNA and activity along the rat colon and have analyzed the distribution of 11 beta-HSD, MR, and glucocorticoid receptor (GR) mRNA within rat distal colon using in situ hybridization. Levels of 11 beta-HSD mRNA (1.7 and 3.4 kb) and activity were higher in distal vs. proximal colon, paralleling reported MR mRNA levels. Within the distal colon mucosa both 11 beta-HSD immunoreactivity and mRNA was observed in cells in the lamina propria but not in epithelial cells. MR mRNA was present in surface epithelial cells, but was also colocalized with the same 11 beta-HSD-expressing cells in the lamina propria. In contrast GR mRNA was more uniformly distributed. The localization of MR mRNA to nonepithelial cells in the lamina propria, possibly neuroendocrine cells, suggests that mineralocorticoid-regulated sodium transport across colonic epithelial cells may also involve a paracrine mechanism. As with the kidney, exposure of active mineralocorticoid to the MR in these cells in the lamina propria is dictated by 11 beta-HSD in an autocrine fashion.

Diet-derived nutrients mediate the inhibition of hypothalamic NPY neurons in the arcuate nucleus of mice during refeeding

2009 ◽  
Vol 297 (1) ◽  
pp. R100-R110 ◽  
Author(s):  
Csilla Becskei ◽  
Thomas A. Lutz ◽  
Thomas Riediger
Keyword(s):  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Peptide Yy ◽  
Small Reduction ◽  
Hypothalamic Arcuate Nucleus ◽  
Ad Libitum ◽  
Fos Expression

Fasting activates orexigenic neuropeptide Y neurons in the hypothalamic arcuate nucleus (ARC) of mice, which is reversed by 2 h refeeding with standard chow. Here, we investigated the contribution of diet-derived macronutrients and anorectic hormones to the reversal of the fasting-induced ARC activation during 2 h refeeding. Refeeding of 12-h-fasted mice with a cellulose-based, noncaloric mash induced only a small reduction in c-Fos expression. Refeeding with diets, containing carbohydrates, protein, or fat alone reversed it similar to chow; however, this effect depended on the amount of intake. The fasting-induced ARC activation was unchanged by subcutaneously injected amylin, CCK (both 20 μg/kg), insulin (0.2 U/kg and 0.05 U/kg) or leptin (2.6 mg/kg). Insulin and leptin had no effect on c-Fos expression in neuropeptide Y or proopiomelanocortin-containing ARC neurons. Interestingly, CCK but not amylin reduced the ghrelin-induced c-Fos expression in the ARC in ad libitum-fed mice, suggesting that CCK may inhibit orexigenic ARC neurons when acting together with other feeding-related signals. We conclude that all three macronutrients and also non-nutritive, ingestion-dependent signals contribute to an inhibition of orexigenic ARC neurons after refeeding. Similar to the previously demonstrated inhibitory in vivo action of peptide YY, CCK may be a postprandial mediator of ARC inhibition.

scholarly journals Preparation and characteristics of gelatin sponges crosslinked by microbial transglutaminase

PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e3665 ◽  
Author(s):  
Haiyan Long ◽  
Kunlong Ma ◽  
Zhenghua Xiao ◽  
Xiaomei Ren ◽  
Gang Yang
Keyword(s):  
Cell Proliferation ◽  
Water Absorption ◽  
Crosslinking Agent ◽  
Microbial Transglutaminase ◽  
High Porosity ◽  
Cell Compatibility ◽  
High Viability ◽  
Good Biocompatibility ◽  
The Stability

Microbial transglutaminase (mTG) was used as a crosslinking agent in the preparation of gelatin sponges. The physical properties of the materials were evaluated by measuring their material porosity, water absorption, and elastic modulus. The stability of the sponges were assessed via hydrolysis and enzymolysis. To study the material degradation in vivo, subcutaneous implantations of sponges were performed on rats for 1–3 months, and the implanted sponges were analyzed. To evaluate the cell compatibility of the mTG crosslinked gelatin sponges (mTG sponges), adipose-derived stromal stem cells were cultured and inoculated into the scaffold. Cell proliferation and viability were measured using alamarBlue assay and LIVE/DEAD fluorescence staining, respectively. Cell adhesion on the sponges was observed by scanning electron microscopy (SEM). Results show that mTG sponges have uniform pore size, high porosity and water absorption, and good mechanical properties. In subcutaneous implantation, the material was partially degraded in the first month and completely absorbed in the third month. Cell experiments showed evident cell proliferation and high viability. Results also showed that the cells grew vigorously and adhered tightly to the sponge. In conclusion, mTG sponge has good biocompatibility and can be used in tissue engineering and regenerative medicine.

In vivo application of decellularized rat colon and evaluation of the engineered scaffolds following 9 months of follow‐up

2020 ◽  
Vol 44 (11) ◽  
pp. 2253-2262
Author(s):  
Abdol‐Mohammad Kajbafzadeh ◽  
Kiarad Fendereski ◽  
Reza Khorramirouz ◽  
Seyedeh Sima Daryabari ◽  
Ahmad Masoomi ◽  
...  
Keyword(s):  
Rat Colon
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