Mechanisms of intestinal adaptation: unstirred layer resistance and membrane transport

1984 ◽  
Vol 62 (6) ◽  
pp. 678-682 ◽  
Author(s):  
A. B. R. Thomson
Keyword(s):  
Kinetic Parameters ◽  
Molecular Mechanisms ◽  
Intestinal Adaptation ◽  
Intestinal Transport ◽  
Lauryl Alcohol ◽  
Transport Processes ◽  
Unstirred Layer ◽  
Incremental Change ◽  
Medium Chain Length ◽  
Acute And Chronic Exposure

The effect of the resistance of unstirred water layers (UWL) on the kinetic parameters of active and passive intestinal transport processes is well established, but the possibility of adaptive changes in the resistance of this diffusion barrier in health and disease has only recently been appreciated. The rate of uptake (Jd) of a homologous series of saturated fatty alcohols into the jejunum is limited by diffusion through the UWL. The Jd of lauryl alcohol has been determined at different rates of stirring of the bulk phase and at different sites along the intestine, in animals of different ages, in varying species, in rats with streptozotocin-induced diabetes mellitus, following abdominal irradiation, after acute and chronic exposure to ethanol and after the feeding of various diets. The UWL varies in response to most of these experimental manipulations. After correcting for unstirred layer effects, the incremental change in free energy (∫ΔFW → l) of the uptake of medium chain-length fatty acids and the maximal transport rate ([Formula: see text]) and Michaelis constant (Km) for glucose uptake were determined. These kinetic parameters changed in many of these experimental manipulations. However, there was no correlation between changes in UWL, ∫ΔFw → l, [Formula: see text], Km or [Formula: see text]/Km. It is concluded that (1) the intestine is capable of adapting to a variety of physiological and pathological challenges; and (2) the major kinetic changes included UWL, ∫ΔFW → l[Formula: see text] and Km. The molecular mechanisms responsible for these changes in the dimensions and characteristics of the barriers to intestinal transport must now be defined.

Kinetics of uptake of glucose in rabbit jejunum: influence of sodium, unstirred layers, and passive permeation

1983 ◽  
Vol 61 (10) ◽  
pp. 1129-1137 ◽  
Author(s):  
A. B. R. Thomson
Keyword(s):  
Glucose Uptake ◽  
Intestinal Transport ◽  
Water Layer ◽  
Lauryl Alcohol ◽  
Unstirred Layer ◽  
Transport Rate ◽  
Rabbit Jejunum ◽  
Layer Resistance ◽  
Kinetics Of Uptake

Failure to account for the effect of the unstirred water layer and the contribution of passive permeation will lead to errors in the estimation of the kinetic constants of glucose uptake into the intestine. It is widely accepted that variations in the concentration of sodium in the bulk phase profoundly influence the rate of uptake of glucose in the intestine, but the kinetic basis for this effect remains in dispute. Accordingly, a previously validated in vitro technique was used to assess the effect of Na+ on the uptake of glucose into rabbit jejunum under conditions selected to reduce the unstirred layer resistance. Varying Na+ had no effect on the uptake of lauryl alcohol and therefore on unstirred layer resistance. The passive permeability coefficient for glucose uptake was estimated from the uptake of L-glucose, of D-glucose at 4 °C, or in the presence of 1 mM phlorizin or 40 mM galactose. The permeability for glucose increased as Na+ rose. The values of both the maximal transport rate and the Michaelis constant (Km) were influenced by Na+. A linear relationship was noted between Na+ and the maximal transport rate; the value of Km fell as Na+ was increased to 75 mequiv./L, but Km did not decline further with higher values of Na+. These results support the theoretical predictions of the presence of both an affinity and a velocity effect of the sodium gradient on the intestinal transport system for glucose.

Claudin Tight Junction Proteins: Novel Aspects in Paracellular Transport

2008 ◽  
Vol 28 (6) ◽  
pp. 577-584 ◽  
Author(s):  
Constanze Will ◽  
Michael Fromm ◽  
Dominik Müller
Keyword(s):  
Tight Junction ◽  
Solute Transport ◽  
Molecular Mechanisms ◽  
Family Members ◽  
Transport Processes ◽  
Paracellular Transport ◽  
Solute Flux ◽  
Solute Fluxes ◽  
Essential Components ◽  
Renal Tubular

Claudins are essential components of the intercellular tight junction and major determinants of paracellular solute fluxes across epithelia and endothelia. Many members of this family display a distinct charge or size specificity, whereas others render the epithelium impermeable to transport. Due to intercellular localization, claudin-mediated transport processes are passive and driven by an electrochemical gradient. In epithelial tissues, claudins exhibit a temporal–spatial expression pattern corresponding with regional and local solute transport profiles. Whereas paracellular transport mechanisms in organs such as intestine and kidney have been extensively investigated, little is known about the molecular mechanisms determining solute transport in the peritoneum, and thus the determinants of peritoneal dialysis. Given the ubiquitous expression of claudins in endothelia and epithelia, it is predictable that claudins also contribute to pore formation and determination in the peritoneum, and that they are involved in solute flux. Therefore, we review the basic characteristics of claudin family members and their function as exemplified in renal tubular transport and give an outlook to what extent claudin family members might be of importance for solute reabsorption across the peritoneal membrane.

Regulation of intestinal glucose transport

1992 ◽  
Vol 70 (9) ◽  
pp. 1201-1207 ◽  
Author(s):  
D. J. Philpott ◽  
J. D. Butzner ◽  
J. B. Meddings
Keyword(s):  
Small Intestine ◽  
Glucose Transport ◽  
Intestinal Adaptation ◽  
Basolateral Membrane ◽  
Intestinal Transport ◽  
Glucose Absorption ◽  
Dietary Carbohydrate ◽  
Adaptive Responses ◽  
Carbohydrate Levels ◽  
Specific Regulation

The small intestine is capable of adapting nutrient transport in response to numerous stimuli. This review examines several possible mechanisms involved in intestinal adaptation. In some cases, the enhancement of transport is nonspecific, that is, the absorption of many nutrients is affected. Usually, increased transport capacity in these instances can be attributed to an increase in intestinal surface area. Alternatively, some conditions induce specific regulation at the level of the enterocyte that affects the transport of a particular nutrient. Since the absorption of glucose from the intestine is so well characterized, it serves as a useful model for this type of intestinal adaptation. Four potential sites for the specific regulation of glucose transport have been described, and each is implicated in different situations. First, mechanisms at the brush-border membrane of the enterocyte are believed to be involved in the upregulation of glucose transport that occurs in streptozotocin-induced diabetes mellitus and alterations in dietary carbohydrate levels. Also, factors that increase the sodium gradient across the enterocyte may increase the rate of glucose transport. It has been suggested that an increase in activity of the basolaterally located Na+–K+ ATPase could be responsible for this phenomena. The rapid increase in glucose uptake seen in hyperglycemia seems to be mediated by an increase in both the number and activity of glucose carriers located at the basolateral membrane. More recently, it was demonstrated that mechanisms at the basolateral membrane also play a role in the chronic increase in glucose transport observed when dietary carbohydrate levels are increased. Finally, alterations in tight-junction permeability enhance glucose absorption from the small intestine. The possible signals that prompt these adaptive responses in the small intestine include glucose itself and humoral as well as enteric nervous interactions.Key words: intestinal transport, glucose transport, intestinal adaptation.

scholarly journals Changes in porcine nutrient transport physiology in response to Ascaris suum infection

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Sarina Koehler ◽  
Andrea Springer ◽  
Nicole Issel ◽  
Stefanie Klinger ◽  
Christina Strube ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Ascaris Suum ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Nutrient Transport ◽  
Transport Processes ◽  
Infected Group ◽  
Peptide Transporter ◽  
Control Group ◽  
Expression Levels

Abstract Background The roundworm Ascaris suum is one of the parasites with the greatest economic impact on pig farming. In this context, lower weight gain is hypothesized to be due to decreased nutrient absorption. This study aims at characterizing the effects of A. suum infection on intestinal nutrient transport processes and potential molecular mechanisms. Methods Three groups of six piglets each were infected orally (10,000 embryonated A. suum eggs) in a single dose (“single infection”). Another three groups were infected orally (1000 embryonated eggs) for 10 consecutive days (“trickle infection”). Animals were necropsied 21, 35 and 49 days post-infection (dpi). Three groups served as respective controls. The Ussing chamber technique was applied for the functional characterization of small intestinal tissues [short-circuit currents (Isc) as induced by glucose, alanine and peptides; 3H-glucose net flux rates; tissue conductance (Gt)]. Transcription and expression levels of relevant cytokines and nutrient transporters were evaluated (qPCR/western blot). Results Peptide- and alanine-induced changes in Isc were significantly decreased in the jejunum and ileum of the trickle-infected group at 49 dpi and in the ileum of the single-infected group at 49 dpi. No significant differences regarding glucose transport were observed between the Ascaris-infected groups and the control group in Ussing chamber experiments. Transcription levels of the glucose and peptide transporters as well as of selected transcription factors (transcription of signal transducer and activator of transcription 6 [STAT6] and hypoxia-inducible factor 1-alpha [Hif-1α]) were significantly increased in response to both infection types after some periods. The transcription of interleukins 4 and 13 varied between decrease and increase regarding the respective time points, as did the protein expression of glucose transporters. The expression of the peptide transporter PepT1 was significantly decreased in the ileal single-infected group at 35 dpi. Hif-1α was significantly increased in the ileal tissue from the single-infected group at 21 dpi and in the trickle-infected group at 35 dpi. The expression levels of Na+/K+-ATPase and ASCT1 remained unaffected. Conclusions In contrast to the current hypothesis, these results indicate that the nutrient deprivation induced by A. suum cannot be explained by transcriptional or expression changes alone and requires further studies. Graphical abstract

Effect of chronic ingestion of ethanol on in vitro uptake of lipids and glucose in the rabbit jejunum

1984 ◽  
Vol 246 (2) ◽  
pp. G120-G129
Author(s):  
A. B. Thomson
Keyword(s):  
Fatty Acids ◽  
Food Intake ◽  
Weight Control ◽  
Bulk Phase ◽  
Unstirred Layer ◽  
Control Group ◽  
Cholesterol Uptake ◽  
Incremental Change ◽  
Rabbit Jejunum

This study was undertaken to determine the effect of chronic feeding of ethanol on the in vitro jejunal uptake of lipids and glucose. The first group of rabbits was fed ad libitum (CAL); the food intake of a second control group [weight control (WC)] was restricted to match their gain in body weight with that of a chronically ethanol-fed group (ETH); and the food intake of a third control group [food control (FC)] was restricted to match the food intake with that of ETH. There was a marked decline in cholesterol uptake in WC and FC compared with CAL, and cholesterol uptake in ETH was intermediate between the higher value in CAL and the lower value in WC and FC. The uptake of fatty acids 4:0-12:0 was similar in the CAL, FC, WC, and ETH groups, both when the bulk phase was stirred and unstirred; the uptake of fatty acids 16:0 and 18:0 was lower in WC and FC than in CAL; and the uptake of fatty acids 14:0, 16:0, and 18:0 was even lower in ETH. The uptake of a homologous series of fatty alcohols was greater in WC and ETH than in CAL at five different rates of stirring of the bulk phase. When the uptake of fatty acids 6:0-12:0 was corrected for unstirred layer resistance, a linear relation was noted between fatty acid chain length and the natural logarithm of rate of uptake/aqueous diffusion coefficient, and the steeper slope in WC and ETH than in CAL represented a higher incremental change in free energy. Glucose uptake was similar in CAL, WC, and FC but was greater in ETH from 5 to 40 mM glucose. These studies demonstrate that 1) weight restriction, food restriction, and chronic ethanol feeding are associated with a change in the effective resistance of the unstirred layer and in the passive permeability properties of the rabbit jejunum, and 2) ethanol has a differential effect on passive permeation of short-, medium-, and long-chain fatty acids and cholesterol.

scholarly journals ‘Candidatus Phytoplasma solani’ interferes with the distribution and uptake of iron in tomato

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Sara Buoso ◽  
Laura Pagliari ◽  
Rita Musetti ◽  
Marta Martini ◽  
Fabio Marroni ◽  
...  
Keyword(s):  
Plant Pathogens ◽  
Molecular Mechanisms ◽  
Transcriptional Response ◽  
Transcriptome Profiling ◽  
Transport Processes ◽  
Fe Deficiency ◽  
Cultivated Plants ◽  
Chlorophyll Metabolism ◽  
Wide Range ◽  
Phytoplasma Infection

Abstract Background ‘Candidatus Phytoplasma solani’ is endemic in Europe and infects a wide range of weeds and cultivated plants. Phytoplasmas are prokaryotic plant pathogens that colonize the sieve elements of their host plant, causing severe alterations in phloem function and impairment of assimilate translocation. Typical symptoms of infected plants include yellowing of leaves or shoots, leaf curling, and general stunting, but the molecular mechanisms underlying most of the reported changes remain largely enigmatic. To infer a possible involvement of Fe in the host-phytoplasma interaction, we investigated the effects of ‘Candidatus Phytoplasma solani’ infection on tomato plants (Solanum lycopersicum cv. Micro-Tom) grown under different Fe regimes. Results Both phytoplasma infection and Fe starvation led to the development of chlorotic leaves and altered thylakoid organization. In infected plants, Fe accumulated in phloem tissue, altering the local distribution of Fe. In infected plants, Fe starvation had additive effects on chlorophyll content and leaf chlorosis, suggesting that the two conditions affected the phenotypic readout via separate routes. To gain insights into the transcriptional response to phytoplasma infection, or Fe deficiency, transcriptome profiling was performed on midrib-enriched leaves. RNA-seq analysis revealed that both stress conditions altered the expression of a large (> 800) subset of common genes involved in photosynthetic light reactions, porphyrin / chlorophyll metabolism, and in flowering control. In Fe-deficient plants, phytoplasma infection perturbed the Fe deficiency response in roots, possibly by interference with the synthesis or transport of a promotive signal transmitted from the leaves to the roots. Conclusions ‘Candidatus Phytoplasma solani’ infection changes the Fe distribution in tomato leaves, affects the photosynthetic machinery and perturbs the orchestration of root-mediated transport processes by compromising shoot-to-root communication.

Influence of vascular and luminal hexoses on rat intestinal basolateral glucose transport

1994 ◽  
Vol 72 (4) ◽  
pp. 317-326 ◽  
Author(s):  
Raymond Tsang ◽  
Ziliang Ao ◽  
Chris Cheeseman
Keyword(s):  
Glucose Transport ◽  
Plasma Glucose ◽  
Intestinal Adaptation ◽  
Basolateral Membrane ◽  
Physiological Role ◽  
Intestinal Transport ◽  
Membrane Vesicles ◽  
Luminal Perfusion

The influence of luminal and vascular hexoses in rats on glucose transport across the jejunal basolateral membrane (BLM) was measured using isolated membrane vesicles prepared from infused animals. In vivo vascular infusions of glucose produced an increase in glucose transport across BLM vesicles. Sucrose, mannose, galactose, and fructose had no significant effect. Plasma glucose concentrations were unaffected by galactose and sucrose vascular infusions, while mannose and fructose produced a modest rise, and glucose increased plasma glucose to 20 mM. Insulin release was significantly increased by vascular infusion of glucose and fructose, while mannose produced only a small sustained rise. Sucrose and galactose had no effect. Perfusion through the lumen of the rat jejunum in vivo, for up to 4 h, with glucose, fructose, sucrose, or lactate (100 or 25 mM) produced a significant increase in the maximal rate of glucose transport (up to 4- to 5-fold) across BLMs. Galactose and mannose had no effect. Luminal glucose perfusion produced a small nonsignificant increase in glucose inhibitable cytochalasin B binding to BLM vesicles, and no change was seen in the microsomal pool of binding sites. The abundance of GLUT2 in the jejunal BLM, as determined by Western blotting, was unaffected by luminal perfusion of 100 mM glucose for 4 h. Fructose almost completely inhibited the carrier-mediated uptake of glucose in control and upregulated jejunal BLM vesicles. These results are discussed in relation to the physiological role of the upregulation of GLUT2 activity by luminal and vascular hexoses.Key words: intestinal transport, basolateral membrane, glucose transport, intestinal adaptation.

Adaptation of small intestinal membrane transport processes during diabetes mellitus in rats

1990 ◽  
Vol 68 (5) ◽  
pp. 630-635 ◽  
Author(s):  
Richard N. Fedorak
Keyword(s):  
Diabetes Mellitus ◽  
Specific Binding ◽  
Intestinal Transport ◽  
Transport Processes ◽  
Diabetic Rat ◽  
Transport Capacity ◽  
Disease States ◽  
Glucose Binding ◽  
Intestinal Membrane ◽  
Intestinal Hypertrophy

Intestinal amino acid and glucose transport is increased in various disease states and physiological circumstances. This enhancement is generally due to an increase in transport capacity (Vmax) without a change in carrier affinity (KD). Furthermore, the increase in transport capacity is too large to be attributed, in most cases, to simple intestinal hypertrophy. In the streptozotocin-treated chronically diabetic rat model, specific binding indicated an enhanced total number of glucose carriers in the small intestine compared with controls. Furthermore, autoradiography reveals that specific phlorizin (i.e., glucose) binding extends into the intervillous region of the intestine, while in age-matched controls binding is confined to the villous tip. These studies suggest that during experimental diabetes mellitus in rats, enhanced intestinal nutrient absorption may occur as a consequence of recruitment of carriers into previously nontransporting enterocytes. This review looks at ways in which this alteration may be influenced, and examines the expression of various isoforms of Na–K ATPase during streptozocin-induced diabetes mellitus.Key words: intestinal transport, glucose, sodium–potassium ATPase, adaptation.

Sign in / Sign up

Export Citation Format

Share Document