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Department of Veterinary Physiology, Leipzig University, D-04103 Leipzig, Germany and * Department of Animal Nutrition, CCS Haryana Agricultural University, Hisar-125004, India
3To whom correspondence should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • ruminants • sheep • rumen • carbohydrates • sodium glucose-linked transport (SGLT)
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). The
SCFA are directly absorbable across the forestomach wall and cover
80% of the total energy demand of ruminants (Bergman 1990
). Therefore, the current understanding of ruminant
nutrition proceeds from the assumption that the nutritional value of
carbohydrates is determined almost exclusively by their intraruminal
conversion rates to SCFA (Bergman 1990
, Merchen 1988
, Titus and Ahearn 1992
). An
energy-sparing direct use of carbohydrates is believed to be
achievable only by increasing the amount of starch resistant to ruminal
fermentation, i.e., by favoring postruminal starch hydrolysis
(Harmon 1992
, Nocek and Tamminga 1991
).
Postruminal (i.e., intestinal) starch hydrolysis will release glucose
that is directly absorbable via sodium glucose-linked transport
(SGLT-1) across the intestinal epithelium (Krehbiehl et al. 1996
, Shirazi-Beechey et al. 1991
). In the
forestomach itself, however, a direct absorption of glucose has not
been considered to date (Britton and Krehbiel 1993
,
Merchen 1988
), mainly because glucose uptake by ruminal
microbes is very efficient and glucose concentrations in the ruminal
fluid are therefore usually very low (<0.7 mmol/L, Kajikawa et al. 1997
).
In contrast to the above-described paradigm, we recently identified
the expression of the secondary active glucose transporter, SGLT-1, in
the ruminal epithelium (Aschenbach et al. 2000
). In
vitro, the ruminal SGLT-1 had a high affinity to glucose
(Michaelis-Menten constant, K0.5 = 0.28 mmol/L,
Aschenbach et al. 2000
), suggesting its principal
suitability for glucose absorption even at very low intraruminal
concentrations of the substrate. Consequently, the question arises
whether the SGLT-1 identified in vitro is able to eliminate large
quantities of glucose from the rumen in vivo or whether it is simply a
phylogenetic/ontogenetic remnant with no physiologic importance. To
address this question, we measured the glucose disappearance from the
washed and temporarily isolated reticulorumen of sheep. Assessment of
glucose absorption was performed both at a low glucose concentration
that might be expected when feeding standard fiber-based diets
(<0.7 mmol/L, Kajikawa et al. 1997
) and at a high
glucose concentration that might occur after feeding large amounts of
easily fermentable carbohydrates (>10 mmol/L, Ganter et al. 1993
). In addition to a quantitative assessment of glucose
absorption, the experimental setups were designed to show whether the
suspected glucose absorption was occurring via SGLT-1. Criteria for
identifying SGLT-1-dependent glucose absorption were
Na+-dependence, substrate inhibition by galactose
and electrogenicity (Hediger and Rhoads 1994
).
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Experiments were approved by the Regierungspräsidium Leipzig
(TVV-No: 13/97). Adult sheep (Ovis aries, three males
and three females, 60.7 ± 5.8 kg) of the Merino breed were fitted
with a permanent, plugged ruminal fistula (
7.5–9 cm). Sheep had
fully recovered from surgery and completed wound healing before the
start of experiments. They had free access to good quality meadow hay
(first cut), mineral blocks and water. Additionally, sheep received 200
g/d of concentrate (Table 1
) at 0800 h.
|
. In brief,
the esophagus was occluded by the insertion of a saliva collector with
an inflatable cuff 10 cm orally to the cardia. The saliva collector
was held in place by a flexible nasoesophageal probe. The constantly
sucked off saliva was infused into the omasum via a balloon catheter
which, at the same time, isolated the reticulorumen from the omasum and
the distal digestive tract. First experimental setup.
The first experimental series consisted of two independent experiments performed in a 3-wk interval. In each of these two experiments, glucose disappearance from 2 L of the three different experimental buffer solutions, A, B, and C (see section on Buffer solutions), was measured consecutively. Buffer sequence was varied in a total crossover design between sheep and was switched over between the first and second experiment in the same sheep.
During the experiments, each buffer exchange included the removal of the previous buffer solution and two washings with the buffer to be applied. After introduction of the experimental buffer and the start of the 70-min experimental period, the fistula opening was closed and 10-mL samples of the intraruminal solution were taken at 10, 40 and 70 min through polypropylene tubing. The samples were split in two 5-mL aliquots. The first aliquot was immediately frozen in liquid nitrogen, whereas the second aliquot was kept in an agitated water bath (100 oscillations/min) at 38°C under constant gassing with 100% CO2. The aliquot incubated in the water bath was frozen in liquid nitrogen when the next sample was taken out of the reticulorumen, i.e., 30 min later. It served to check for absorption-independent disappearance of glucose from the buffer solutions, especially to check for microbial glucose utilization.
Second experimental setup.
Two months after the first experimental series, the same sheep were used in a second series, except for one female. After washing and isolating the reticulorumen as described above, the hexose-free buffer D (see section on Buffer solutions) was instilled into the reticulorumen and the fistula opening was closed. An infusion bridge (Ringer’s lactate, 1 mL/min) was established into the vena jugularis externa. The potential difference (Pd) between the infusion bridge and the intraruminal buffer solution (transruminal Pd) was measured via KCl-agar bridges and Argenthal reference electrodes (Mettler Toledo, Urdorf, Switzerland) and computed by a flatbed recorder (BD 111, SCI-TEC Instruments/Kipp & Zonen, Saskatoon, Canada). Transruminal Pd remained stable after 30 min of equilibration. Thereafter, the following consecutive additions (final concentrations) were made to the intraruminal buffer: 10 mmol/L D-mannitol at 10 min; 12 mmol/L D-glucose at 20 min; and 20 mmol/L K+ gluconate at 60 min. Two buffer samples were drawn at 25 and 55 min for analysis. An aliquot (5 mL) of the 25-min sample was incubated in a water bath as described above.
Buffer solutions.
The cleansing solution contained 115 mmol/L NaCl, 25 mmol/L NaHCO3 and 10 mmol/L propionic acid (280 ± 5 mosmol/kg; pH 6.7 ± 0.1, initial values). Experimental buffer solution A contained 70 mmol/L NaCl, 25 mmol/L NaHCO3, 5 mmol/L K2HPO4, 2 mmol/L CaCl2, 2 mmol/L MgCl2, 15 mmol/L Na+ acetate, 15 mmol/L Na+ propionate, 15 mmol/L butyric acid, 10 mmol/L D-mannitol and 0.5 mmol/L D-glucose (285 ± 5 mosmol/kg; pH 6.3 ± 0.1, initial values). Experimental buffer solution B had the same composition as buffer solution A except that all sodium ions were replaced by choline. Experimental buffer solution C also resembled buffer solution A except that 10 mmol/L D-mannitol was replaced by 10 mmol/L D-galactose. The totally hexose-free buffer solution D differed from buffer solution A in that 70 mmol/L chloride ions was replaced by gluconate and the initial osmolality was lowered to 275 ± 5 mosmol/kg due to the omission of D-glucose and D-mannitol. The reduction of chloride ions in the last-mentioned solution was intended to decrease the influence of reticuloruminal anion absorption on Pd. All solutions were prewarmed to 38°C and pregassed with 100% CO2 before reticuloruminal infusion. Within the reticulorumen, buffer solutions were constantly gassed and agitated by CO2 bubbling.
The buffer solutions applied during the experimental periods contained
the sodium salts of the antibiotics, cefuroxime (100 mg/L) and colistin
methanesulfonate (25 mg/L). Antibiotics were chosen because of their
broad efficacy against the gastrointestinal microflora (Song and Glenny 1998
, Spath and Hirner 1998
) and because
their chemical structure did not suggest interaction with SGLT-1.
Furthermore, a chromic EDTA (Cr:EDTA) solution (10 mL/L) was added to
the experimental solutions as a fluid marker. Cr:EDTA solution was
prepared as follows: 179 mmol CrCl3 was dissolved in 300 mL
of distilled water and 179 mmol Na2EDTA was dissolved in
500 mL of distilled water. Thereafter, both solutions were mixed and
boiled together for 1 h. After the mixture was cooled to room
temperature, 13 mmol CaCl2 was added. Finally, the pH was
adjusted to 6.0 using 10 mol/L NaOH and the volume was adjusted to 1 L
using distilled water.
After addition of antibiotics and Cr:EDTA, measured sodium concentrations were 127.7 ± 0.5, 10.4 ± 0.6 and 127.7 ± 0.4 mmol/L and chromium concentrations were 1.54 ± 0.03, 1.58 ± 0.03 and 1.59 ± 0.02 mmol/L for buffers A, B and C, respectively. In buffer D, only chromium concentration was determined, which was 1.44 ± 0.4 mmol/L.
Sample analysis.
Chromium and sodium concentrations were measured by atomic absorption spectrophotometry (AAS Solar 929, ATI Unicam, Cambridge, UK). Glucose concentrations were determined by the hexokinase method, using the Hitachi 704 analyzer (Hitachi Instruments, San Jose, CA; reagents by Roche Diagnostics, Mannheim, Germany). Galactose concentrations were determined photometrically (Spekol 11, Zeiss, Jena, Germany) by the galactose dehydrogenase method, using the Lactose/D-Galactose determination system of Roche Diagnostics.
Presentation of results and statistical analysis.
Solute quantities were corrected for dilution effects on the basis of the concentration changes of the fluid marker, Cr:EDTA. The results of the two independent experiments in the first experimental period were pooled for buffer solution and animal before calculation of the respective mean of all sheep. All means are arithmetic and presented together with their standard error of mean (SEM) and the number of single/pooled observations (n). Time-dependent changes of solute concentrations or Pd were assessed by Student’s paired t test. Comparisons between solute changes in different buffer solutions were performed either by Student’s unpaired t test or by one-way ANOVA and Tukey’s test as appropriate. All calculations and statistical tests were performed by the computer programs Microsoft Excel 5.0 (Microsoft, Redmond, WA) or Jandel SigmaStat 2.0 (SPSS, Chicago, IL).
Chemicals.
CO2 was supplied by Messer Griesheim (Krefeld, Germany). Galactose, colistin methanesulfonate and choline chloride were purchased from Fluka (Buchs, Switzerland). All other chemicals were obtained either from Merck (Darmstadt, Germany) or from Sigma-Aldrich (Deisenhofen, Germany).
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Portions of the buffer samples drawn from the reticulorumen were
incubated ex vivo (38°C, CO2 gassing) for 30
min. This procedure served to exclude the possibility that the hexose
disappearance rates measured in vivo would represent microbial hexose
utilization rather than reticuloruminal hexose absorption. No glucose
and galactose disappeared from the samples during the ex vivo
incubations (data of first samples, Fig. 1
; data of following samples not shown). Consequently, microbial growth
and metabolism in the buffer solutions were effectively inhibited by
the washing procedures and the antimicrobial treatment in both
experimental series.
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Glucose absorption was measured and characterized at the low luminal
glucose concentration of 0.5 mmol/L in the first experimental series.
Under control conditions, a considerable portion of glucose disappeared
(P < 0.01) in two consecutive 30-min periods
(buffer A, Fig. 2A
). Glucose disappearance rates from buffer A were 0.060 ± 0.011
and 0.070 ± 0.017 mmol/30 min in the first and second periods,
respectively (n = 6). This was 6.3 ± 1.2 and 7.7
± 1.6% of the glucose amount present intraruminally at the
beginning of the respective 30-min periods. To test whether the
disappearance rates measured from buffer A occurred in a
sodium-dependent manner via the epithelial SGLT-1, glucose
disappearance was also determined at low Na+
concentrations (buffer B) and in the presence of the competitive
inhibitor of SGLT-1, galactose (buffer C). Glucose disappearance was
completely inhibited when the intraruminal Na+
concentration was reduced from 128 to 10 mmol/L (buffer B, Fig. 2A
). On the other hand, measurable glucose disappearance
occurred in the presence of 10 mmol/L galactose (at 128 mmol/L
Na+), but only if a 1-h period was considered
(buffer C, Fig. 2A
). Accordingly, the 1-h glucose
disappearance tended to be smaller (P = 0.31) in the
presence (0.096 ± 0.037 mmol/h) compared with the absence (0.130
± 0.020 mmol/h) of galactose (buffer C vs. buffer A, Fig. 2A
). Disappearance of galactose from buffer C was not
detectable (Fig. 2B
).
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Because the results at 0.5 mmol/L glucose strongly supported the
presence of reticuloruminal Na+/glucose
cotransport, one goal of the second experimental series was to
visualize the glucose-induced Na+ currents
via their influence on the transruminal Pd. The control application of
10 mmol/L mannitol (final concentration) to a hexose-free buffer
solution had no influence on the transruminal Pd (Fig. 3A
). In contrast, the subsequent addition of 12 mmol/L glucose to the
intraruminal buffer D increased Pd from 34.4 ± 1.7 to 37.1
± 1.9 mV within 4 min (P < 0.001; n =
5). The increase in Pd coincided with a glucose disappearance rate of
2.87 ± 0.85 mmol/30 min (i.e., 11.0 ± 3.0%/30 min;
P < 0.05; Fig. 3B
). At 60 min, the proper
function of the Pd-recording equipment was verified by the
induction of a K+ diffusion potential. The
luminal addition of 20 mmol/L K+ gluconate
induced an increase in Pd from 37.3 ± 2.0 to 41.3 ± 1.1 mV
within 1 min (P < 0.05; Fig. 3A
).
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Changes in the reticuloruminal fluid volume were calculated from changes in the chromium concentrations in all experiments because the absorption of solutes, including hexoses, across the reticuloruminal epithelium might potentially be linked to transeptithelial water fluxes, i.e., solvent drag. In the presence of 0.5 mmol/L glucose in the first experimental series, there were no significant changes in the reticuloruminal fluid volume. In the presence of 12 mmol/L glucose in the second experimental series, there was a trend for a small reduction in the reticuloruminal fluid volume (by 3.3 ± 1.3%/30 min; P = 0.082). However, the latter relative decrease in fluid volume was much smaller (P < 0.05) than the concurrent decrease in the relative amount of reticuloruminal glucose (by 11.0 ± 3.0%/30 min).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Glucose disappearance was identified from the washed and temporarily
isolated reticulorumen of sheep. The observed glucose disappearance was
totally dependent on the luminal Na+
concentration (Fig. 1A
), which points to active and
sodium-coupled elimination of glucose from the forestomach lumen.
However, active glucose uptakes by bacteria (Kajikawa et al. 1997
) and by mammalian epithelial cells (Hediger and Rhoads 1994
, Shirazi-Beechey et al. 1991
) are
both sodium-coupled. Therefore, clear evidence was required that
glucose disappearance would represent ruminal glucose absorption and
not microbial metabolism. The experimental setups were designed
accordingly because the forestomach model used is largely but not
totally free of ruminal microbes (especially of those adhering to the
reticuloruminal wall). First, antibiotics were added in a combination
and concentrations that are effective against most of the
gastrointestinal bacteria (Song and Glenny 1998
,
Spath and Hirner 1998
). Second, the efficacy of the
antibiotic treatment against microbial glucose utilization was verified
by control incubations of ruminal buffer samples ex vivo (Fig. 1)
.
Third, the undetectable disappearance of galactose (Fig. 2B
)
compared with glucose (Fig. 2A
,
Fig. 3B
) also
disproved microbial fermentative activity (including fermentation by
microbes attached to the reticuloruminal wall) because ruminal microbes
should be able to utilize not only glucose but also galactose
(reticuloruminal galactose digestibility during feeding of orchard
grass hay in a 500-kg steer is 600 mmol/d, i.e., 93.7% of the total
tract galactose digestibility, calculated from Bourquin et al. 1994
). Finally, direct evidence for reticuloruminal glucose
absorption was provided by visualizing the currents induced by the
electrogenic cotransfer of Na+ across the
reticuloruminal wall via its contribution to the transruminal Pd (Fig. 3A
). In this case, false-positive results (i.e., Pd
increases due to osmotic effects) were excluded by the control
application of mannitol. The model was also protected against
false-negative results (i.e., failure of the Pd-recording
equipment), which would have been detectable due to a missing Pd
increase after elevation of the intraruminal K+
concentration.
Given the clear evidence concerning Na+-coupled
glucose absorption across the reticuloruminal epithelium, earlier in
vitro studies suggested that SGLT-1 should be the responsible transport
protein (Aschenbach et al. 2000
). To verify the function
of SGLT-1 in vivo, we tried to inhibit glucose absorption competitively
by the addition of galactose, a physiologic substrate of SGLT-1 in many
species (Hediger and Rhoads 1994
). A small,
nonsignificant inhibition of glucose absorption by galactose (Fig. 2A
) suggested that absorption is probably linked to SGLT-1.
This presupposes, however, that galactose was a poor substrate for
ovine SGLT-1.
Assuming SGLT-1 to be the transporter in charge, the question arises
whether forestomach glucose absorption is mediated exclusively by this
membrane protein. A hypothesis was proposed by Pappenheimer and Reiss (1987)
in which the bulk flow of glucose across the
intestinal epithelium takes place only to a small extent on the
transcellular route via SGLT-1. Instead, the "Pappenheimer
hypothesis" states that the principal route for intestinal glucose
transport is by solvent drag through paracellular channels. The latter
is thought to occur secondarily to the transcellular (i.e.,
translateral) absorption of the osmolytes, Na+
and glucose, and an opening of the paracellular junctions. In the
present study using the reticulorumen, paracellular solvent drag was
not the major route of glucose absorption on the basis of the small,
nonsignificant changes in the reticuloruminal fluid volume. One may
suspect some minor disappearance of glucose by solvent drag only at the
high glucose concentration of 12 mmol/L.
Delivery of metabolic energy.
When assuming a metabolic energy value of 2816 kJ/mol glucose
(Kleiber 1961
), the energy intake due to forestomach
glucose absorption was 0.17 kJ/30 min at a glucose concentration of 0.5
mmol/L, or 8 kJ/d. For comparison, total metabolizable energy intake
is on the order of 10 MJ/d in a 60-kg sheep during summer grazing of
grass-based paddocks [473 kJ/(kg0.75·d),
Herselman et al. 1999
]. Consequently, reticuloruminal
absorption of glucose would theoretically account for <0.1% of the
metabolizable energy intake during roughage feeding. At the high
intraruminal glucose concentration of 12 mmol/L, however, glucose
disappearance would be equivalent to 387 kJ/d or 4% of the daily
metabolizable energy intake. Therefore, forestomach glucose absorption
may reach energetic importance at luminal glucose concentrations in the
millimolar range. The latter conclusion also takes into consideration
that the results of the present experiments are likely to underestimate
grossly the real energetic contribution of forestomach glucose
absorption. First, the reticulorumen was filled with only 2 L of buffer
solution, meaning that the major part of the epithelium was not in
contact with buffer solution and did not take part in absorption.
Second, there is another forestomach compartment distal to the
reticulorumen, the omasum, which may potentially also absorb glucose
(Ganter et al. 1993
). Third, the relative energy value
of glucose in comparison to SCFA is much higher in ruminants than in
monogastric species because ruminants rely almost completely on
gluconeogenesis to meet their glucose demands (Reynolds et al. 1994
). A direct absorption of glucose will therefore decrease
the animal’s metabolic expenditure for gluconeogenesis.
Currently, many efforts are being made to enhance the energy intake of
ruminants by feeding increasing amounts of easily fermentable
carbohydrates (Dann et al. 1999
, Heldt et al. 1999
). Unfortunately, few data exist on ruminal glucose
profiles under these "preacidotic" feeding conditions.
Forestomach glucose concentrations are usually not measured in
feeding trials. However, information on the concentration profiles of
free glucose in the ruminal content is essential to perform absorption
studies in the practically relevant concentration range and to make a
final judgment on the energetic importance of forestomach glucose
absorption. In principal, this study has demonstrated that sheep are
able to extract much more than 6 mmol/h glucose from the forestomach
contents at a glucose concentration of 12 mmol/L. Absorptive capacities
for glucose are therefore not tremendously different between the
forestomach and the small intestine of sheep. For comparison,
White et al. (1971)
found that the maximal intestinal
glucose absorption of adult sheep (determined at an initial luminal
concentration of 166 mmol/L) varies between 21 mmol/h (grazing animals)
and 43 mmol/h (concentrate-fed animals, 100 g lucerne chaff plus
500 g whole wheat grain).
Stabilization of the ruminal ecosystem.
Reticuloruminal glucose absorption was present in the sheep used although the pre-experimental diet was a maintenance diet with only some concentrate. Consequently, the high clearance of luminal glucose at a concentration of 12 mmol/L suggests that reticuloruminal epithelia may effectively counteract sudden increases in the luminal glucose concentration, even in animals not adapted to large amounts of easily fermentable carbohydrates. By decreasing the luminal availability of free glucose, forestomach epithelia counteract the microbial dysfermentation that would lead to severe illness, i.e., ruminal lactic acidosis. Therefore, sodium-coupled absorption of glucose has to be considered a defense mechanism against the genesis of ruminal acidosis. It remains to be shown in further studies whether this defense mechanism may be upregulated long-term when adapting high yielding animals to high energy diets.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Supported by the Deutsche Forschungsgemeinschaft
(DFG: Ga 329/3–1). S.K.B. received a grant of the German Academic
Exchange Service (DAAD).
4 Abbreviations used: Pd, potential difference;
SCFA, short-chain fatty acids; SGLT, sodium glucose-linked
transport.
Manuscript received April 25, 2000. Initial review completed June 1, 2000. Revision accepted August 2, 2000.
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