scholarly journals The Effect of Potassium on the Intestinal Transport of Glucose

1966 ◽  
Vol 50 (1) ◽  
pp. 113-128 ◽  
Author(s):  
T. Z. Csáky ◽  
P. M. Ho
Keyword(s):  
Small Intestine ◽  
Specific Activity ◽  
Lactic Acid Production ◽  
Sugar Transport ◽  
Intestinal Transport ◽  
Intestinal Lumen ◽  
High K ◽  
Rate Of Absorption ◽  
Specific Sugar

The rate of absorption of glucose, galactose, and 3-0-methylglucose was studied in the rat's small intestine perfused in situ with isosmotic solutions containing these sugars and Na2SO4 or K2SO4. The presence of high [K+] in the lumen enhances absorption of glucose but not that of galactose or of 3-0-methylglucose. The potassium stimulation is apparent at higher glucose concentrations where primarily carrier-mediated diffusion is involved in the translocation. In this case potassium stimulates transport even if it is the only cation in the lumen. The potassium-stimulated intestine produces more glycogen with higher specific activity than the control gut. Lactic acid production by the intestine is markedly enhanced if the intestinal lumen is perfused with a solution containing glucose and high [K+]. It is concluded that potassium does not affect permeability or the specific sugar transport system of the gut, but enhances intracellular metabolic disappearance of glucose thereby creating a larger luminal intracellular concentration gradient which in turn enhances the rate of carrier-facilitated entry.

Absorption of beta-casomorphins from autoperfused lamb and piglet small intestine

1990 ◽  
Vol 259 (3) ◽  
pp. G443-G452 ◽  
Author(s):  
L. C. Read ◽  
A. P. Lord ◽  
V. Brantl ◽  
G. Koch
Keyword(s):  
Small Intestine ◽  
Intestinal Lumen ◽  
Physiological Conditions ◽  
Naturally Occurring ◽  
Gut Epithelium ◽  
Measured Absorption ◽  
Beta Casein ◽  
Kinetics Of

beta-Casomorphins (beta-CMs) derived from milk beta-casein may exert various opiate activities in milk-fed infants. To assess the physiological significance of beta-CMs as a source of circulating opioids in infants, we measured absorption rates of several beta-CMs under near-physiological conditions using in situ autoperfused lamb intestine. The naturally occurring beta-CMs, beta-CM-7 and beta-CM-4-amide, were absorbed readily into blood with no transfer into lymph. Uptake peaked within several minutes of the luminal infusion of peptide but then declined sharply and stopped within a further 10-15 min. The recovery in blood, intestinal contents, and tissue at the end of the 30-min experiment was less than 1% of the infused dose. The low recovery was due to rapid proteolysis based on in vitro studies that demonstrated half-lives of less than 5 min in lamb blood, luminal contents, and lymph. The synthetic dipeptidyl peptidase IV-resistant analogue beta-[D-Ala2]CM- 4-amide was stable during incubation in blood, lymph, or luminal contents and was absorbed into blood at rates that were maximal within several minutes and remained steady for the 30-min period. We conclude that although natural beta-CMs are transferred across the lamb small intestine, rapid degradation within the intestinal lumen, gut epithelium, and blood would prevent entry into the circulation under normal conditions. Val-beta-CM-7, a putative stable precursor, had similar stability and kinetics of absorption to beta-CM-7, results that exclude Val-beta-CM-7 as a stable precursor for delivery of beta-CMs to the circulation. Essentially identical results to those in lambs were obtained in 7-day-old piglets.

Fate of dietary glutathione: disposition in the gastrointestinal tract

1990 ◽  
Vol 259 (4) ◽  
pp. G530-G535 ◽  
Author(s):  
T. M. Hagen ◽  
G. T. Wierzbicka ◽  
B. B. Bowman ◽  
T. Y. Aw ◽  
D. P. Jones
Keyword(s):  
Small Intestine ◽  
Gastrointestinal Tract ◽  
Intestinal Lumen ◽  
Glutathione Disulfide ◽  
Semisynthetic Diet ◽  
Gamma Glutamyltransferase ◽  
Physiological Importance ◽  
Fasted Rats ◽  
Absorption Measurements

Studies were performed in rats that had been fasted 24 h, fed a glutathione (GSH)-free semisynthetic diet (AIN-76), and fed the same diet supplemented with GSH. The results from the fasted rats and those fed GSH-free diet showed that the duodenum and jejunum contained 0.2-0.5 mumol of GSH/gram wet wt of luminal contents. The GSH contents of biliary juice was sufficient to maintain this amount of GSH in the intestinal lumen. Other analyses showed that cell sloughing, bacterial GSH content, and GSH secretion by epithelial cells of the jejunum were not sufficient to account for this content. GSH concentrations following consumption of a GSH-supplemented diet (5-50 mg/g AIN-76) showed a rapid increase in all regions of the small intestine and indicated that removal occurred primarily in the jejunum. However, the combined activities of brush-border gamma-glutamyltransferase and GSH uptake systems were not sufficient to remove all of the ingested GSH. Results from in situ vascular perfusions of small intestine showed that the upper jejunum is a principal site of GSH absorption. Measurements of the GSH-to-glutathione disulfide (GSSG) ratio in the lumen after ingestion of GSSG (5 mg/g diet) indicated that the upper small intestine also has a mechanism for reducing GSSG to GSH. The results therefore indicate that GSH is present in the lumen of the small intestine of rat under most if not all conditions. Although the physiological importance of luminal GSH remains unclear, it could potentially be used to detoxify reactive electrophiles in the diet or be absorbed for intracellular detoxication reactions.

scholarly journals Part of quercetin absorbed in the small intestine is conjugated and further secreted in the intestinal lumen

1999 ◽  
Vol 277 (1) ◽  
pp. G120-G126 ◽  
Author(s):  
Vanessa Crespy ◽  
Christine Morand ◽  
Claudine Manach ◽  
Catherine Besson ◽  
Christian Demigne ◽  
...  
Keyword(s):  
Small Intestine ◽  
Intestinal Wall ◽  
Intestinal Lumen ◽  
Intestinal Cells ◽  
Biliary Duct ◽  
In Situ Perfusion ◽  
Perfusion Period ◽  
Hydrolysis Of

Rutin and quercetin absorption and metabolism were investigated in rats after in situ perfusion of jejunum plus ileum (15 nmol/min). In contrast to rutin, a high proportion of quercetin (two-thirds) disappeared during perfusion, reflecting extensive transfer into the intestinal wall. Net quercetin absorption was not complete (2.1 nmol/min), inasmuch as 52% were reexcreted in the lumen as conjugated derivatives (7.7 nmol/min). Enterohepatic recycling contribution of flavonoids was excluded by catheterization of the biliary duct before perfusion. After a 30-min perfusion period, 0.71 μM of quercetin equivalents were detected in plasma, reflecting a significant absorption from the small intestine. The differential hydrolysis of effluent samples by glucuronidase and/or sulfatase indicates that the conjugated forms released in the lumen were 1) glucuronidated derivatives of quercetin and of its methoxylated forms (64%) and 2) sulfated form of quercetin (36%). In vitro quercetin glucuronides synthetized using jejunal and ileal microsomal fractions were similar to those recovered in the effluent of perfusion. These data suggest that glucuronidation and sulfatation take place in intestinal cells, whereas no glucurono-sulfoconjugates could be detected in the effluent. The present work shows that a rapid quercetin absorption in the small intestine is very effective together with its active conjugation in intestinal cells.

Neurotensin stimulates [3H]oleic acid translocation across rat small intestine

1986 ◽  
Vol 251 (6) ◽  
pp. G823-G829 ◽  
Author(s):  
M. J. Armstrong ◽  
M. C. Parker ◽  
C. F. Ferris ◽  
S. E. Leeman
Keyword(s):  
Small Intestine ◽  
Oleic Acid ◽  
Mesenteric Artery ◽  
Specific Activity ◽  
Femoral Vein ◽  
Lymph Flow ◽  
Entire Length ◽  
Intestinal Lumen ◽  
Rat Small Intestine ◽  
Series Of Experiments

The effect of neurotensin (NT) on the translocation of intraluminally administered lipid across the duodenum as well as across the entire length of the small intestine was studied in the rat. In the first series of experiments, the appearance in the lymph of [3H]oleic acid instilled as a bolus into a segment of the duodenum was followed for 3 h. Infusion of NT (0.6 pmol X kg-1 X min-1) via the superior mesenteric artery resulted in a significant increase in the appearance of label in the lymph when compared with saline infusion (17.3 +/- 3.1 vs. 8.6 +/- 1.4%, P less than 0.01, respectively). In the second series of experiments, lipid was infused into the entire length of the small intestine over 4 h, and the accumulation of label in the lymph was measured. The infusion of NT (1.0 pmol X kg-1 X min-1) into the femoral vein also significantly increased the appearance of label when compared with animals infused with saline (49.0 +/- 2.0 vs. 34.2 +/- 5.2%, P less than 0.05, respectively). In this study, the specific activity of the triglyceride recovered in the lymph was higher in the rats given NT than in the controls (P less than 0.05). No significant changes in lymph flow were observed as a consequence of NT infusion. These results indicate that NT infusion into the circulation increases the translocation of oleic acid from the intestinal lumen into the lymph of rats.

Prolylhydroxyproline Absorption in Hamsters

1972 ◽  
Vol 50 (7) ◽  
pp. 782-790 ◽  
Author(s):  
H. J. Hueckel ◽  
Q. R. Rogers
Keyword(s):  
Small Intestine ◽  
Absorption Rate ◽  
Intestinal Transport ◽  
Intestinal Wall ◽  
Relative Resistance ◽  
Rate Of Absorption ◽  
Small Intestines ◽  
Mucosal Side ◽  
Active Reabsorption

The intestinal transport of the dipeptide prolylhydroxyproline was investigated using hamsters and segments of hamster small intestines. The feeding of prolylhydroxyproline to hamsters resulted in the urinary excretion of 2% of the ingested dipeptide after 3 h or 7% after 24 h. In vitro perfusions of prolylhydroxyproline through the hamster small intestine resulted in the movement of the dipeptide across the intestinal wall. The rate of absorption was proportional to the concentration of prolylhydroxyproline on the mucosal side (0.17 μmol Pro∙Hyp/mM in lumen/g tissue/h). Anoxia, 2,4-dinitrophenol, cyanide, or an excess of proline or hydroxyproline did not change this absorption rate. These results suggest that prolylhydroxyproline is absorbed by "simple passive diffusion", that it reaches the site of intestinal absorption because of its relative resistance to enzymatic hydrolysis, and that it is excreted by glomerular filtration without subsequent active reabsorption.

Renal interstitial Ca2+

2000 ◽  
Vol 278 (4) ◽  
pp. F644-F649 ◽  
Author(s):  
Maria M. Mupanomunda ◽  
Bing Tian ◽  
Norio Ishioka ◽  
Richard D. Bukoski
Keyword(s):  
Small Intestine ◽  
Wistar Rats ◽  
Interstitial Fluid ◽  
Muscle Tone ◽  
Intestinal Lumen ◽  
Kidney Cortex ◽  
Proximal Small Intestine ◽  
Mean Diameter

Renal interstitial fluid Ca2+concentration ([Ca2+]isf) was measured in anesthetized Wistar rats by using in situ microdialysis. During perfusion of 20 cm of the proximal small intestine with Ca2+-free buffer, renal [Ca2+]isf was 1.63 ± 0.19 mmol/l in the cortex ( n = 6) and 1.93 ± 0.12 mmol/l in the medulla ( n = 5, P = 0.223). When Ca2+ in the intestinal lumen was increased to 3 mmol/l, no change was seen in total or ionized serum Ca2+(SCa), urinary Ca2+ excretion (UCa), or Ca2+ in a microdialysate of the kidney cortex. Increasing intestinal Ca2+ further, to 6 mmol/l, was without effect on SCa but significantly increased UCa by 38% and microdialysate Ca2+by 36% (1.25 ± 0.0.09 vs. 1.70 ± 0.14 mmol/l, n = 4, P < 0.05). Intravenous infusion of 28 ng ⋅ kg− 1 ⋅ min− 1of parathyroid hormone for 1 h during perfusion of the intestinal lumen with 1 mmol/ Ca2+caused a 7–10% rise in SCa, a 40% fall in UCa, and a 32% increase in microdialysate Ca2+ (1.32 ± 0.13 vs. 1.74 ± 0.13 mmol/l, n = 6, P < 0.05). Interlobar arteries with a mean diameter of 120 μm were studied by using a wire myograph to determine whether changes in extracellular Ca2+ affect muscle tone. When precontracted with 5 μmol/l serotonin, the arteries relaxed in response to cumulative addition of Ca2+(1–5 mmol/l) with an ED50 value for Ca2+of 3.30 ± 0.08 mmol/l, n = 3. These data demonstrate that [Ca2+]isf changes dynamically during manipulation of whole-animal Ca2+ homeostasis and that intrarenal arteries relax in response to extracellular Ca2+ varied over the range measured in vivo.

Dietary and developmental regulation of intestinal sugar transport

2001 ◽  
Vol 360 (2) ◽  
pp. 265-276 ◽  
Author(s):  
Ronaldo P. FERRARIS
Keyword(s):  
Small Intestine ◽  
Glucose Transport ◽  
Molecular Mechanisms ◽  
Glucose Transporter ◽  
De Novo ◽  
Sugar Transport ◽  
Transport Systems ◽  
Intestinal Lumen ◽  
Transport Activity ◽  
Cellular Mechanisms

The Na+-dependent glucose transporter SGLT1 and the facilitated fructose transporter GLUT5 absorb sugars from the intestinal lumen across the brush-border membrane into the cells. The activity of these transport systems is known to be regulated primarily by diet and development. The cloning of these transporters has led to a surge of studies on cellular mechanisms regulating intestinal sugar transport. However, the small intestine can be a difficult organ to study, because its cells are continuously differentiating along the villus, and because the function of absorptive cells depends on both their state of maturity and their location along the villus axis. In this review, I describe the typical patterns of regulation of transport activity by dietary carbohydrate, Na+ and fibre, how these patterns are influenced by circadian rhythms, and how they vary in different species and during development. I then describe the molecular mechanisms underlying these regulatory patterns. The expression of these transporters is tightly linked to the villus architecture; hence, I also review the regulatory processes occurring along the crypt-villus axis. Regulation of glucose transport by diet may involve increased transcription of SGLT1 mainly in crypt cells. As cells migrate to the villus, the mRNA is degraded, and transporter proteins are then inserted into the membrane, leading to increases in glucose transport about a day after an increase in carbohydrate levels. In the SGLT1 model, transport activity in villus cells cannot be modulated by diet. In contrast, GLUT5 regulation by the diet seems to involve de novo synthesis of GLUT5 mRNA synthesis and protein in cells lining the villus, leading to increases in fructose transport a few hours after consumption of diets containing fructose. In the GLUT5 model, transport activity can be reprogrammed in mature enterocytes lining the villus column. Innovative experimental approaches are needed to increase our understanding of sugar transport regulation in the small intestine. I close by suggesting specific areas of research that may yield important information about this interesting, but difficult, topic.

In situ demonstration of migration of dendritic cells released from rat small intestine to mesenteric lymph nodes

2001 ◽  
Vol 120 (5) ◽  
pp. A183-A183
Author(s):  
H KOBAYASHI ◽  
H NAGATA ◽  
S MIURA ◽  
T AZUMA ◽  
H SUZUKI ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Small Intestine ◽  
Lymph Nodes ◽  
Rat Small Intestine ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph

Histological examination of rat small intestine after surgical removal of obturation small bowel obstruction and peptide stimulation of lymph flow

2018 ◽  
pp. 157-162
Author(s):  
А.А. Коваленко ◽  
Г.П. Титова ◽  
В.К. Хугаева
Keyword(s):  
Small Intestine ◽  
Surgical Treatment ◽  
Survival Rate ◽  
Small Bowel ◽  
Goblet Cells ◽  
Intestinal Wall ◽  
Structure And Function ◽  
Lymph Flow ◽  
Intestinal Lumen ◽  
And Function

Оперативное лечение различных заболеваний кишечника сопровождается осложнениями в виде нарушений микроциркуляции в области анастомоза кишки. Ранее нами показана способность лимфостимуляторов пептидной природы восстанавливать нарушенную микроциркуляцию, что послужило основой для настоящего исследования. Цель работы - оценка влияния стимуляции лимфотока в стенке кишки на процессы восстановления микроциркуляции, структуры и функции тонкой кишки в области оперативного вмешательства. Методика. В экспериментах на наркотизированных крысах (хлоралгидрат в дозе 0,6 г/кг в 0,9% растворе NaCl) моделировали различные поражения тонкой кишки (наложение лигатуры, перевязка 1-3 брыжеечных артерий, перекрут петли кишки вокруг оси брыжейки, сочетание нескольких видов повреждений). Резекция поврежденного участка через 1 сут. с последующим созданием тонкокишечного анастомоза завершалась орошением операционного поля раствором пептида-стимулятора лимфотока (40 мкг/кг массы животного в 1 мл 0,9% раствора NaCl). На 7-е сут. после операции проводили гистологическое исследование фрагмента кишки в области анастомоза. Результаты. На 7-е сут. после резекции у выживших животных (летальность вследствие кишечной непроходимости составляла 30%) имеют место морфологические признаки острых сосудистых нарушений стенки кишки, изменений кровеносных и лимфатических микрососудов, интерстициальный отек всех слоев стенки кишки, дилатация просвета кишки, повреждение всасывающего эпителия ворсин с истончением щеточной каемки клеток, морфологические признаки гиперфункции бокаловидных клеток. Использование лимфостимулятора пептидной природы после операции увеличивало выживаемость животных на 24%. У части животных отмечалось уменьшение расширения просвета кишки, у других практически полная его нормализация. Восстанавливалась форма кишечных ворсин и распределение бокаловидных клеток. Отсутствовали признаки внутриклеточного и межмышечного отека. Отмечено умеренное полнокровие венул. Заключение. Использование лимфостимулятора при хирургическом лечении кишечной непроходимости увеличивает выживаемость животных на 24% по сравнению с контролем, способствует более раннему восстановлению структуры и функции тонкой кишки. Полученные результаты свидетельствуют о перспективности использования стимуляции лимфотока при операциях на кишечнике. Surgical treatment of bowel diseases is associated with complications that cause microcirculatory disturbances in the anastomosis area and may lead to a fatal outcome. This study was based on our previous finding that peptide-type lymphatic stimulators are able to restore impaired microcirculation. The aim of this work was stimulating the lymph flow in the intestinal wall to facilitate recovery of microcirculation, structure and function of the small intestine in the area of surgical intervention. Methods. In experiments on anesthetized rats (0.6 g/kg chloral hydrate in 0.9% NaCl), various small bowel lesions were modeled (bowel ligation, ligation of 1-3 mesenteric arteries, gut torsion, combination of several lesion types). In 24 h, the damaged area was resected, and a small intestine anastomosis was creased. The surgery was completed with irrigation of the operative field with a solution of lymph flow stimulating peptide (40 мg/kg body weight in 1 ml of 0.9% NaCl). A gut fragment from the anastomosis area was examined histologically on day 7 after the surgery. Results. On the 7th day after removing the intestinal obstruction, the surviving animals (lethality 30%) had morphological signs of acute vascular disorders in the intestinal wall; changes in blood and lymphatic microvessels; interstitial edema of all intestinal wall layers; dilatation of the intestinal lumen; damage to the absorptive epithelium of villi with thinning of the brush border, and hyperfunction of mucous (goblet) cells. The use of the peptide after surgery increased the survival rate of animals by 24% and provided a smaller dilatation of the intestinal lumen in some animals. In other animals, the lumen recovered. The shape of intestinal villi and distribution of goblet cells were restored. Signs of intracellular and intermuscular edema were absent. Moderate venular congestion was noticed. Conclusion. Using the lymphatic stimulator in surgical treatment of intestinal obstruction increases the survival rate of animals by 24% compared to the control, facilitates earlier restoration of the small intestine structure and function. The obtained results indicated the effectiveness of lymphatic stimulation in intestinal surgery.

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