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J. Anim. Sci. 2002. 80:2740-2746
© 2002 American Society of Animal Science

Influence of food deprivation on the transport of 3-O-methyl-{alpha}-D-glucose across the isolated ruminal epithelium of sheep

G. Gäbel1 and J. R. Aschenbach

Veterinär-Physiologisches Institut, Universität Leipzig, D-04103 Leipzig, Germany

1 Correspondence:
An den Tierkliniken 7 (phone: ++49-341-9738061; fax: ++49-341-9738097; E-mail:
gaebel{at}rz.uni-leipzig.de).


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Implications
 Literature Cited
 
Recent studies provided evidence that the ruminal epithelium is able to absorb D-glucose even at physiologically low intraruminal concentrations. To elucidate whether ruminal D-glucose transport shows adaptive responses during food deprivation, transport of 3-O-methyl-{alpha}-D-glucose (3-OMG), a hardly metabolizable D-glucose analogue, was measured in isolated ruminal epithelia obtained from hay-fed or food-deprived adult sheep. In both groups, a significant net absorption of 3-OMG to the serosal side (in vivo: blood side oriented) could be detected at 3-OMG concentrations between 0.25 mM and 5 mM. Net absorption of 3-OMG was abolished by mucosal (in vivo: lumen side oriented) addition of phlorizin, an inhibitor of the sodium glucose-linked transporter 1 (SGLT-1). Net absorption of 3-OMG followed Michaelis-Menten kinetics, but apparent affinity and maximal transport capacity were lower in epithelia obtained from food-deprived sheep. In contrast to the decrease of the (secondary) active 3-OMG transport, serosal-to-mucosal permeation of 3-OMG increased after food deprivation, suggesting an elevated passive 3-OMG transfer. It is concluded that the altered transport characteristics are either part of a global energy-sparing process during food deprivation (i.e., a lowered activity of the Na+/K+-ATPase) or result from specific down-regulation of SGLT-1.

Key Words: Adaptation • Forestomach • Glucose Absorption • Intraepithelial Metabolism • Sheep


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Implications
 Literature Cited
 
Nutritional value of carbohydrates for ruminants is assumed to be almost exclusively determined by their intraruminal conversion rates to short-chain fatty acids (Bergman, 1990; Merchen, 1988). However, recent studies identified the transcription and functional expression of the secondary active glucose transporter, SGLT-1, in ruminal epithelium of sheep (Zhao et al., 1998; Aschenbach et al., 2000b). SGLT-1 is able to absorbD-glucose efficiently from the rumen of sheep adapted to a standard hay and concentrate diet (Aschenbach et al., 2000a).

In the intestines of many species, SGLT-1 is known to be regulated by lack of luminal nutrient availability. However, results are controversial. In lambs and calves, expression of the intestinal SGLT-1 decreases dramatically in correspondence with the decline in luminal sugars after weaning (Shirazi-Beechey et al., 1991; Wood et al., 2000). By contrast, studies in mice suggested that chronic (270 d) energy restriction of mice is coupled to an increased capacity for intestinal D-glucose transport, whereas acute energy restriction (1 to 10 d) has no effect on murine nutrient absorption at all (Ferraris et al., 2001).

Ruminants are often inadvertently deprived of feed over short periods of time in the existing production and marketing systems, implying a drastic decrease in the amount of nutrients available for absorption (Galyean et al., 1981; Gäbel et al., 1993). Luminal changes are accompanied by alterations in epithelial function. After 48 h of food deprivation, capacity of the reticulorumen to absorb electrolytes drastically decreases (Gäbel et al., 1993). We hypothesized that activity of the ruminal SGLT-1 could also change during this time scale. Therefore, transport of the SGLT-1 substrate, 3-O-methyl-{alpha}-D-glucose (3-OMG), was compared between isolated ruminal epithelia obtained from sheep either fed at maintenance or deprived of food for 48 h. Possible changes in absorptive area were assessed in parallel.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Implications
 Literature Cited
 
Animals and Feeding
Twelve female Merino sheep, aged 10 to 18 mo at the beginning of the experiment, were used. They were fed hay (20 g/kg BW). The chemical composition of hay was analyzed by a commercial laboratory (AGRUB, Markleeberg, Germany) according to Naumann and Bassler (1997). The hay with 92.4% DM contained (% of dry matter): CP, 10.1; crude fat, 2.5; crude fiber, 29.3; ash, 7.6; NFE, 50.5; NDF, 63.3; ADF, 33.8; ADL, 26.8; hemicellulose, 29.6; cellulose, 7.0; reducing sugars after inversion (calculated as saccharose equivalent), 5.8; starch, 0.0. Tap water and a salt block were freely available. After a prefeeding period of at least 3 wk, animals were divided into two groups of six sheep with matching weight distribution. To determine the effects of food deprivation, food was withdrawn in one group 48 h before slaughter. The six sheep of the other group had access to hay until 30 min before slaughter. Experimental procedures were approved by the Regierungspräsidium Leipzig (TVV-No. 13/97).

Preparation of the Ruminal Epithelium
Animals were killed by exsanguination after stunning, and the reticulorumen was removed from the abdominal cavity 3 to 10 min later. A piece (150 cm2) of the ventral ruminal sac was cut out of the ruminal wall and washed carefully. According to Gäbel et al. (1991), isolated ruminal epithelium was prepared by removing the serosal and muscular layers. Epithelia washing, preparation, and subsequent transport to the laboratory were performed in the standard buffer solution described below. The solution was kept at 37°C and bubbled with 95% O2/5% CO2. The isolated mucosa was cut into squares (approximately 3 x 3 cm2) and mounted between two Lucite half-chambers (Ussing chambers) with an inner aperture of 3.14 cm2. Edge damage was minimized by rings of silicon rubber on both sides of the tissue. The bathing solutions on both sides of the mucosa were circulated by gas lift and maintained at 37°C in water-jacketed reservoirs.

Electrical Measurements
Electrophysiological measurements were conducted according to Aschenbach et al. (2000b). The transepithelial potential difference (PDt) was measured using Argenthal reference electrodes (Mettler Toledo, Urdorf, Switzerland) connected to the half-chambers by bridges containing 3% agar constituted in 3% KCl. Current was applied by a computer-controlled voltage clamp device (Ing.-Büro für Mess- und Datentechnik, Aachen, Germany) via a second set of electrodes (Ag-AgCl electrodes and 0.9% NaCl/3% agar bridges). Before mounting of epithelia, junction potential and fluid resistance were determined by the voltage clamp device for later automatic correction of electrophysiological measurements. Epithelia were short-circuited during all experiments, i.e., PDt was clamped to 0 mV. The current needed for zero clamping of PDt is equal but oppositely directed to the short-circuit current (Isc, originating from active epithelial transport of charge). Tissue conductance (Gt) was determined by measuring the changes in transepithelial potential difference during exposure to bipolar impulses of 100 µA for 300 ms at 60-s intervals (Gt = {delta}I/{delta}PDt).

Determination of 3-OMG Fluxes
After mounting, 150 kBq [3H-]3-OMG were added to the mucosal or the serosal side, and epithelia were allowed to adapt to experimental conditions for 30 min. Consequently, all fluxes were determined under steady state conditions. Pairs of epithelial sheets matching in conductance (difference less than 25%) were used for measurement of unidirectional fluxes. Mucosal-to-serosal and serosal-to-mucosal fluxes of 3-OMG were calculated on the basis of radioactivity appearing at the unlabeled side according to Gäbel et al. (1991). Radioactivity was determined by scintillation counting (Wallac 1409 LSC, Berthold, Bad Wilbach, Germany) after addition of scintillation fluid (Aquasafe 300 Plus, Zinsser, Frankfurt, Germany) to the samples.

Solutions
The standard buffer solution used for washing and Ussing chamber experiments contained (in mM): 75 NaCl, 25 NaHCO3, 5 KCl, 2 NaH2PO4, 1 Na2HPO4, 1 CaCl2, 2 MgCl2, 8 NaOH, 5 3-[N-morpholino] propanesulfonic acid (MOPS), 30 sodium gluconate, 10 n-butyric acid; gassed with 95% O2/5% CO2. 3-O-methyl-{alpha}-D-glucose was added until the indicated concentration was reached. In the buffer solutions containing less the 5 mM3-OMG, 3-OMG was equimolarly replaced by mannitol. Further additions are indicated in the figure legends. Initial osmolality of all solutions was determined by freezing point depression (Knauer Osmometer, Berlin, Germany) and adjusted to values between 285 and 291 mosmol • kg-1by adding mannitol. Initial pH was adjusted to values between 7.35 and 7.41.

Morphometry of Surface Area
To determine mucosal surface area, we used a semiquantitative method (Dirksen et al., 1984). From the stripped epithelium of the ventral ruminal sac, five samples with an area of 3.14 cm2 were punched out and fixed with 4% formalin. The number of papillae was counted, and all papillae were cut off thereafter. The surface of one flat side of the papilla was measured by light microscopy with the aid of an electronic planimeter (Reiss Precision 3005, VEB Zentronik, Bad Liebenwerda, Germany). Total surface area of the papilla was assumed to be twice the measured value (i.e., the area of edges was neglected). For statistical analysis, the surface areas of all papillae from one sample were averaged to provide one value per animal. Absorbing surface was calculated according to the formula:


Chemicals
Carbogen (95% O2/5% CO2) was supplied by Messer Griesheim (Krefeld, Germany). The 3-OMG was purchased from DuPont NEN (Bad Homburg, Germany). All other chemicals were obtained either from Merck (Darmstadt, Germany) or from Sigma-Aldrich (Deisenhofen, Germany).

Calculations and Statistical Analysis
The 3-OMG net fluxes at different 3-OMG concentrations were tested for Michaelis-Menten kinetics by fitting to the following equation:


where is the maximal 3-OMG net flux at saturating substrate concentration, [3-OMG] is 3-OMG concentration, and is the 3-OMG concentration at 0.5 . To determine significance of differences between two groups, unpaired Student’st-test was applied. Paired Student’st-test was used to determine differences between unidirectional flux rates of one epithelial pair or differences between consecutive flux periods in the same observational unit. When multiple means were compared, one way analysis of variance (ANOVA) was carried out on the data first. If this indicated a significant difference between means, a Student-Newman-Keuls test was employed to determine which of the means differed from each other. Statistical tests and calculations were performed using Sigma-Stat 2.0 or Sigma Plot 2001 software (Jandel Scientific, San Rafael, CA). Data presented are arithmetic means with their standard error of means (SEM).


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Implications
 Literature Cited
 
Food deprivation did not influence luminal absorptive area. In the epithelial sheets with a serosal area of 3.14 cm2, the mean absorptive surface area on the mucosal side amounted to 6.63 ± 0.72 cm2and to 5.91 ± 0.14 cm2in fed and food-deprived animals, respectively.

In both fed and food-deprived sheep, mucosal-to-serosal flux of 3-OMG was greater (P< 0.05, paired Student’st-test) than the oppositely directed flux at all concentrations tested, i.e., 3-OMG was net absorbed. Since thePDt was clamped to 0 mV and a transepithelial chemical gradient was absent, the observed net absorption indicates the presence of active absorptive mechanisms. To evaluate, whether 3-OMG transport is mediated by SGLT-1, 3-OMG transport was measured in epithelia pre-treated with the inhibitor of SGLT-1, phlorizin (Kimmich, 1990; Ferraris and Diamond, 1986a, b). Simultaneously, control epithelia were preincubated with an equal amount of the phlorizin solvent, ethanol. As shown in Table 1Go, mucosal phlorizin addition decreased net absorption when tested at 0.25 mM 3-OMG both in epithelia obtained from food-deprived and fed animals (Table 1Go). Phlorizin was effective also at 3 mM in epithelia obtained from fed animals. However, it could not affect the already decreased net absorption of 3-OMG in food-deprived animals at this concentration. Phlorizin-induced decreases in were due solely to decreases in , whereas the fluxes in the opposite direction were not altered by the inhibitor (Table 1Go).


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  		Table 1. 3-OMG flux rates and electrophysiological data of isolated ruminal epithelia obtained from fed or food-deprived sheep. 3-O-methyl-{alpha}-D-glucose concentration was either 0.25 or 3 mM on both sides of the epithelia. Flux rates of 3-OMG were determined in parallel either under control conditions or after mucosal addition of 0.1 mM phlorizin
 
The activity of SGLT-1 contributes to the overall charge transfer across the epithelium since it carries 2 Na+ions together with one 3-OMG molecule (Hediger and Rhoads, 1994). Assuming (1) a similar stoichiometry for the ruminal SGLT-1 and (2) totally mediated by SGLT-1, the current coupled directly to SGLT-1 was calculated to be only 14.6% of total short-circuit current at 3 mM3-OMG in hay-fed sheep (Table 1Go). For comparison, SEM ofIscvalues was always > 23% (Table 1Go). Consequently phlorizin-induced changes of SGLT1 activity were not detected by changes ofIsc.

Epithelial ion conductance was lowered by food deprivation. However, in contrast to the lowered ion conductivity, was increased (Table 1Go), suggesting an elevated passive permeation of 3-OMG. Altered passive permeation of 3-OMG, in turn, indicated that active SGLT-1 mediated transport could account for only a portion of 3-OMG fluxes. Therefore, the phlorizin-sensitive part of flux rates was calculated (Fig. 1Go). Food deprivation decreased the phlorizin-sensitive part of and, consequently, the phlorizin-sensitive part of (Fig. 1Go).



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  		Figure 1. Effect of food deprivation on the phlorizin-sensitive flux rates of 3-OMG. Phlorizin-sensitive flux rates were calculated on the basis of the data shown in Table 1Go by subtracting the flux rates determined after phlorizin addition from the flux rates determined under control conditions. Data represent means ± SEM of six sheep. *,**P < 0.05, 0.01 to fed sheep (unpaired Student’s t-test).

 
To determine the kinetics of SGLT-1 transport, the dependence of on substrate concentration was tested. In the absence of phlorizin, increased when elevating the concentration of extracellular 3-OMG from 0.25 mMto 5 mMand subsequently became saturated in conformity with Michaelis-Menten kinetics. Nonlinear regression analysis yielded an apparent of 1.81 ± 0.32 mMand a of 27.4 ± 2.0 nmol • cm-2• h-1in epithelia obtained from hay-fed sheep. In epithelia obtained from food-deprived sheep, the calculated and were lower (P< 0.05) than the respective values of epithelia obtained from fed sheep.

To demonstrate that is attributable solely to 3-OMG transport by SGLT-1, phlorizin was added to all epithelia directly after measuring the above described net flux rates under control conditions. In all epithelia, mucosal addition of 0.1 mMphlorizin completely abolished net transport within 90 min (Fig. 2Go). During the same time period (90 min), remained almost constant in epithelia of fed animals receiving no phlorizin both at 0.25 mM(0 to 60 min, 2.86 ± 0.51 nmol • cm-2• h-1; 90 to 150 min, 3.63 ± 0.80 nmol • cm-2• h-1; n = 6) and 3 mM3-OMG (0 to 60 min, 17.4 ± 1.7 nmol • cm-2• h-1; 90 to 150 min, 19.0 ± 3.5 nmol • cm-2• h-1; n = 6). The same continuity applied to consecutively measuredin phlorizin-free epithelia of food-deprived sheep (data not shown). Consequently, epithelial function remained stable during incubation, and time-dependent decreases incould be excluded in both groups.



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  		Figure 2. Dependence of 3-OMG flux rates on 3-OMG concentration in fed and food-deprived sheep. The 3-OMG concentration was varied on both sides of the epithelium. The line was drawn using a non-linear regression-fitting routine (Marquard-Levenberg algorithm) according to the Michaelis-Menten kinetics formula. Kinetic data are specified in the text. Immediately after determining basal 3-OMG fluxes, 0.1 mM phlorizin was added to the mucosal buffer reservoir. Ninety minutes after the addition of phlorizin, 3-OMG net transport was abolished at any of the concentration tested (open circles), i.e., ms flux was not different from sm flux (paired Student’s t-test). Data represent means ± SEM of six sheep.

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Implications
 Literature Cited
 
D-glucose can be absorbed from the ruminant forestomach by an SGLT-1-mediated process (Zhao et al., 1998; Aschenbach et al., 2000a, b). Moreover, results from our previous studies indicated that SGLT-1 is the only significantD-glucose transporter in the apical membrane of the ruminal epithelium (Aschenbach et al., 2000b), which is similar to the intestine (Wright, 1993, 2001). In these studies (Aschenbach et al., 2000a,b), the predominant role of the ruminal SGLT-1 in glucose transport was concluded from (1) electrogenicity and transport inhibition by phlorizin (thereby excluding apical facilitated glucose transporters; Hediger and Rhoads, 1994; Wright, 1993, 2001), (2) molecular identification of SGLT-1 mRNA, (3) high Na+affinity (thereby excluding SGLT-2; Hediger et al., 1995; Wright, 2001), (4) high glucose affinity; most compatible with SGLT-1; Hediger et al., 1995; Wright, 2001), and (5) the ability to transport 3-OMG. The latter substrate was also chosen in the present study to characterize the function of SGLT-1, because 3-OMG is transported by only SGLT-1 but not SGLT-2 and SGLT-3 (Wright, 2001). A second advantage of 3-OMG is its resistance to enzymatic breakdown (Hopfer, 1987; Shirazi-Beechey, 1996). Thus, transport function of SGLT-1 can be studied without eliciting shifts in cell metabolism.

Taking phlorizin-sensitive 3-OMG net transport as an indicator of SGLT-1 activity, the results shown in Table 1Go and Figure 1Go provided evidence that the activity of the ruminal SGLT-1 can be altered. Alteration could be induced either directly by the lack of energy/substrate supply with the diet and(or) indirectly by alterations of the whole-animal metabolic status. Providing that reflects the maximal transport capacity (Vmax) of SGLT-1, the decreasedVmaxfound in food-deprived animals (Fig. 2Go) can totally account for the lower absorption rates of 3-OMG (Table 1Go). A reduced capacity of SGLT-1 or of glucose transport was also found in the small intestine of food-deprived rats (Kotlet et al., 1980; Debnam, 1982). However, the underlying reasons for the reduced intestinal transport capacity are still under debate. It is an open question whether the changes in kinetic parameters observed during food deprivation result from a reduction in the mass of (absorbing) epithelial cells from alterations in carrier abundance and(or) characteristics, or from changed driving forces during food deprivation (Debnam and Levin, 1975, 1976; Debnam, 1982; Gal-Garber et al., 2000; Ferraris et al., 2001).

As regards morphological alterations in the rumen, our measurements of mucosal surface area do not point to a reduction in epithelial cell mass after 48 h of food deprivation. It is also very unlikely that greater histological changes have occurred since morphology changes much more slowly in the ruminal epithelium compared to the intestine. Depending on the diet, the turnover time for the ruminal epithelium ranges from 5 to 17 d (Goodlad, 1981). In the intestine, the whole process of proliferation in the crypts, upward migration/differentiation, and subsequent exfoliation is completed in 2 to 5 d (Hermiston et al., 1994).

Regulatory changes in carrier abundance and(or) characteristics of the ruminal SGLT-1 would provide a more plausible explanation for the results of the present study. Results from recent investigations on isolated ruminal epithelia indicate that SGLT-1 is under the control of enteroglucagon (Borau et al., 2001). It was demonstrated that the hormone is able to up-regulate apical glucose uptake via SGLT-1 within 15 min. On the other hand, release and turnover of enteroglucagon are reduced by starvation, at least, in laboratory animals (Goodlad et al., 1983; Hoyt et al., 1996). Consequently, a lack of enteroglucagon (or other yet unidentified endocrine signals) during starvation can be expected to down-regulate the ruminal SGLT-1. However, it has to be asked whether the observed short-term control of the ruminal SGLT-1 by enteroglucagon is also effective during a food deprivation lasting for 48 h.

An alternative way of SGLT-1 regulation may be direct modulation by substrates. Shirazi-Beechey and coworkers (1994) showed that D-glucose, several non-metabolizableD-glucose analogues, and even nontransportable analogues ofD-glucose all regulate the expression of the intestinal SGLT-1 protein. In the rumen, a large variety of different hexoses and pentoses, with or without affinity to SGLT-1, can be released by microbial carbohydrate degradation (Scharrer and Grenacher, 2000). It is not evident which of these sugars could potentially regulate the ruminal SGLT-1 under the hay-feeding conditions applied.D-Glucose itself appears to be a poor candidate because intraruminal glucose concentration is very low under physiological feeding conditions (< 0.7 mM; Kajikawa et al., 1997). The pathway of substrate regulation could be transcriptional and(or) posttranscriptional (Lescale-Matys et al., 1993; Shirazi-Beechey et al., 1994; Dyer et al., 1997). Interestingly, the rapid decline of intestinalD-glucose andD-galactose availability in lambs during weaning initiates an almost exclusively posttranscriptional down-regulation of the intestinal SGLT-1 (Lescale-Matys et al., 1993). Thus, posttranscriptional regulation may be the most suitable explanation of the decrease of ruminal SGLT-1 activity in the present study. Transcriptional regulation, on the other hand, would have been hardly effective when assuming a luminal availability of substrates for a certain time after withdrawing feed and a minimum of three d migration time for differentiating cells to reach the proposed apical layer in stratum granulosum (deduced from Goodlad, 1981).

The third possibility for altered SGLT-1 function during food deprivation (i.e., altered driving forces for sugar transport) could also apply to the changes of 3-OMG transport observed in the present study. Reduced driving forces of the ruminal SGLT-1 can result from a diminished activity of the Na+/K+-ATPase, since the pump energizes the electrochemical gradient for the SGLT-1-mediated transport of sugars (Wright, 1993). Na+/K+-ATPase-dependent O2 uptake of the viscera has been shown to decrease after food deprivation (Eisenmann and Nienaber, 1990; McBride and Milligan, 1985). Therefore, a general effect of food deprivation on transport activity of SGLT-1 via a diminished delivery of ATP to the Na+/K+-ATPase may be reflected in a decreased transport of 3-OMG. This assumption is supported by our observation that the of the ruminal SGLT-1 changed concomitantly with the changes ofVmax. Hopfer (1987) and Wright (1993) outlined that the apparent affinity of SGLT-1 for sugar is a function of membrane potential and Na+ concentration. Both of these variables are directly influenced by the activity of the Na+/K+-ATPase (Wright, 1993). Parallel decreases of Vmax and apparent affinity for sugar transport were also observed in earlier studies on the small intestine of food-deprived rats (Debnam, 1982; Debnam and Thompson, 1984).

Food deprivation not only affected (secondary) active sugar absorption. As shown in Table 1Go, was increased in epithelia of food-deprived animals. Since SGLT-1 operates in an absorptive direction (Ferraris and Diamond, 1997), it preferentially influences. The increased flux in the opposite direction (i.e.,thus, likely reflects an elevated part of passive 3-OMG permeation during food deprivation. Elevated passive permeation, in turn, could occur either paracellularly or transcellularly. Increased permeability on the paracellular route is less likely because the paracellular space is ion conductive (Gitter et al., 2000), and ion conductivity decreased during food deprivation (Table 1Go). On the other hand, up-regulation of basolateralD-glucose entry via facilitated transporters (GLUT) could be expected, in food-deprived animals to compensate for the decreased luminal supply of short-chain fatty acids. However, the increased passive 3-OMG flux across the basolateral membrane would only lead to increased transcellular permeation of 3-OMG if facilitated transporters were also present in the apical membrane. Apical and basolateral expression of GLUT-2 has been described in the intestine (Kellett, 2001) but has not been ascertained in the rumen so far.

As concerns the physiological significance of the present results, the lowered activity of SGLT-1 has to be regarded as part of the adaptive response of the organism to a decreased availability of energy. In the food-deprived state, the animal must minimize energy-consuming processes. Since the gastrointestinal tract is a major energy consumer in ruminants (Huntington, 1990; Britton and Krehbiel, 1993; Rémond et al., 1995), decreasing absorptive and metabolic activity of ruminal epithelium contributes to minimizing overall energy expenditure. However, the reduced capacity of the ruminal SGLT-1 may involve negative consequences if intraruminal D-glucose levels suddenly rise after refeeding with carbohydrate-rich diets. In that case, the absorptive processes of the ruminal wall and, in particular, an inefficient SGLT-1 could not sufficiently eliminate acidogenic substrates from the rumen (Aschenbach et al., 2000a). Accordingly, the incidence of ruminal acidosis is higher in animals that are suddenly shifted from the food-deprived state to energy-rich diets (Elam, 1976; Owens et al., 1998; Goad et al., 1998). We propose that this is not only due to insufficient adaptation of the ruminal microflora (Mackie and Gilchrist, 1979) but also due to lower absorptive capacity forD-glucose.


   Implications
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Implications
Literature Cited
 
Our results show that the ruminal D-glucose transport via SGLT-1 is under a dietary and(or) regulatory control. Consequently, avoiding lack of food and keeping certain feeding frequencies ascertains not only the microbial but also the epithelial activity of the forestomach compartment. Thus, the study underlines the rule of never changing the diet when animals had been food deprived before, especially when caloric density needs to be raised. Showing down-regulation in the food-deprived state, further measurements are needed to elucidate whether SGLT-1 might also show adaptive responses in the opposite direction (i.e., whether it is up-regulated) when the animals are accustomed to a high concentrate diet.

Received for publication November 6, 2001. Accepted for publication May 28, 2002.


   Literature Cited
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 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Implications
 Literature Cited
 


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Ferraris, R. P., and J. M. Diamond. 1986a. A method for measuring apical glucose transporter site density in intact intestinal mucosa by means of phlorizin binding. J. Membr. Biol. 94:65–75.[Medline]

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