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Department of Molecular Physiology & Biophysics, Diabetes Research and Training Center and Department of Surgery, Vanderbilt University School of Medicine, Nashville, TN 37232-0615
2To whom correspondence should be addressed. E-mail: r.r.pencek{at}vanderbilt.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • carbohydrate • intestine • phloridzin • dogs
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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–3
). Passive transport occurs via paracellular diffusion across the intestinal wall. Studies have been done to determine the contributions of transporter-mediated and passive processes to total gut glucose absorption. Although some studies using the rat model have shown passive transport to be the major component (4
,5
), other studies in rats and dogs have shown that passive transport is only a minor component compared with transporter-mediated processes (6
,7
). Moreover, little is known about how the contributions of transporter-mediated and passive processes to gut glucose absorption are regulated under physiologic and pathophysiologic conditions.
The purpose of this study was to quantify the contributions of transporter-mediated and passive gut glucose absorption to the blood glucose pool in an in vivo model, i.e., conscious dogs. Assessment of gut glucose absorption in vivo is important because its regulation involves the interaction of hormonal, neural and circulatory mechanisms. The approach described here is an extension of the technique described for rats by Uhing and Kimura (6
). The technique involves the delivery of an intraduodenal tracer bolus containing metabolically inert analogs of D-glucose, i.e., 3-O-[3H]methylglucose (MG; absorbed via active, facilitative, and passive routes) and L-[14C]glucose (L-Glc; absorbed passively) to assess the percentage contributions of transporter-mediated and passive absorption to total gut glucose absorption (8
,9
). The primary difference is that our model allows isotopic methods to be performed in conjunction with arterial, portal and hepatic venous and intraduodenal sampling; blood flows are quantified, and an effort is made to study absorption in the presence of tightly controlled arterial glucose. Additionally, glucose turnover in dogs is the same as in humans, whereas rats have a significantly higher rate of glucose turnover. The dog model also allows for more frequent blood sampling and a more comprehensive assessment of hormones and substrates within the same animal. This technique can be applied to the study of transporter-mediated and passive gut glucose absorption in health and large animal models of disease.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Mongrel dogs of either gender (n = 6) with a mean weight of 23 ± 1 kg were studied. The dogs were housed in a facility that met the American Association for the Accreditation of Laboratory Animals Care guidelines. All procedures were approved by the Vanderbilt University Animal Care and Use Committee. The dogs were fed a standard diet of meat and dry food (34% protein, 14.5% fat, 46% carbohydrate and 5.5% fiber based on dry weight). At least 16 d before each experiment, a laparotomy was performed under general anesthesia. Two silastic catheters (0.03 mm i.d.) were inserted into the inferior vena cava for indocyanine green (ICG) and glucose infusions. Silastic catheters (0.04 mm i.d.) were inserted into the portal vein and left common hepatic vein for blood sampling as described previously. Two silastic catheters (0.03 mm i.d.) were inserted into the duodenum. The first catheter was inserted just below the pyloric sphincter for administration of glucose, phloridzin, MG and L-Glc. The second duodenal catheter was inserted 
10 cm caudal from the infusion catheter (just before the junction of the duodenum with the jejunum). A silastic catheter (0.03 mm i.d.) was inserted into the left femoral artery for blood sampling. After insertion, the vascular catheters were filled with saline containing heparin and knotted at the free ends.
Doppler flow probes (Transonic Systems, Ithaca, NY) were used to measure portal vein and hepatic artery blood flows. A section of the portal vein upstream from the gastroduodenal vein was cleared of tissue and fitted with a 6.0-mm i.d. flow cuff. A section of the hepatic artery was fitted with a 3.0-mm i.d. flow cuff. The flow probe leads and knotted catheter ends were stored in a subcutaneous pocket made in the abdominal region. The femoral artery catheter was stored in a pocket in the inguinal region. Only dogs that met the following criteria were used in this study: a leukocyte count <18,000/mm3, a hematocrit >0.36 by volume, normal stools and a good appetite (consuming the entire daily ration). Dogs meeting these criteria were deprived of food for 18 h before the beginning of the study to ensure that they all were postabsorptive.
Experimental protocol.
The experimental protocol is shown in Figure 1
. On the day of the experiment, the catheters and flow probes were freed from subcutaneous pockets using 2 cm incisions made after application of 2% lidocaine. Saline was infused into the arterial sampling catheter throughout the duration of the study. The dogs were placed in a Pavlov stand and given time to acclimate to the laboratory (t = -190 to -110 min). At t = -110 min, a venous infusion of ICG was initiated and was continued for the duration of the study. This infusion served as a back-up measurement of splanchnic blood flow in case the Doppler probes did not function properly. From t = -30 to 0 min, blood samples were taken for the assessment of baseline measurements. The duodenum was empty during this period and no sample could be obtained. At t = 0 min, the experimental period began with the injection of a 830 µmol/kg glucose primer into the duodenum followed by a continuous intraduodenal infusion of 44 µmol/(kg · min) until t = 90 min. The rate of the intraduodenal glucose infusion was chosen to reproduce glucose levels common in the portal vein after feeding. At t = 20 min, a bolus containing MG and L-Glc (0.925 MBq of each isotope) was injected into the duodenum. At t = 60 min, an intraduodenal bolus of phloridzin (4 µmol/kg) was given followed by a continuous intraduodenal phloridzin infusion of 0.22 µmol/(kg · min) for the remainder of the study. At the start of the phloridzin infusion, an isoglycemic clamp was initiated to maintain the arterial glucose concentration at the level seen before phloridzin infusion. At t = 80 min, a second bolus of MG and L-Glc (3.7 MBq of each isotope), fourfold larger than the first, was introduced into the duodenum. During the experimental period (t = 0 to 90 min), blood and duodenal samples were taken every 10 min. In addition to these samples, blood and duodenum samples were taken every minute for 5 min after administration of each tracer bolus. At the end of the experiment, the dogs were killed with sodium pentobarbital and an autopsy was performed to confirm catheter placement.
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Plasma and intraduodenal glucose levels were determined on the day of the experiment using the glucose oxidase method with a Beckman Glucose Analyzer II (Beckman Instruments, Fullerton, CA). Those plasma samples, which were not immediately analyzed, were stored at -70°C for later analysis. Whole blood and intraduodenal samples were deproteinized with barium hydroxide and zinc sulfate to assess the radioactivity of MG and L-Glc in blood and duodenal samples. After centrifugation at 3000 x g, 30 min, the supernatant was dried and reconstituted in 1 mL of water and 10 mL Ultima Gold scintillant (Packard, Meriden, CT). Radioactivity was determined using a Packard TRI-CARB 2900TR liquid scintillation counter. Plasma insulin and glucagon and blood glucose were measured as described previously (10
).
Calculation.
Total net gut glucose output (NGGO) was determined using Equation 1
.
 | (1) |
where [P] and [A] represent portal vein and arterial glucose concentrations, respectively, and PVF is portal vein blood flow. Calculations of the transporter-mediated and passive components of gut glucose absorption are based upon tracer and glucose data obtained during the 5 min of sampling after administration of the tracer bolus. Due to the inherent uncertainties associated with duodenal sampling, the transporter-mediated and passive components of gut glucose absorption were calculated using three different equations (Equations 2
, 5
and 6)
. The first of these is described by Equation 2
.
 | (2) |
where L-GLCP and L-GLCA represent the portal venous and arterial radioactivity of L-[14C]glucose, respectively. MGP and MGA denote the respective radioactivities of 3-O-[3H]methylglucose in the portal vein and the artery. L-GLCB and MGB represent the radioactivities of each isotope in the bolus injection. The ratio of these two values serves to normalize for different relative amounts of tracer delivered to the duodenum. The remaining radioactivity in the intestine at a given time point (t) was calculated indirectly by subtracting the amount of isotope that has entered the portal vein from the total tracer radioactivity in the initial bolus using Equations 3
and 4
. L-GLCI and MGI represent the indirect calculation of duodenal 3-O-[3H]methylglucose and L-[14C]glucose, respectively.
 | (3) |
 | (4) |
Equation 5
is similar to Equation 2
but instead of being normalized by the amount of tracer in the bolus, the equation is normalized by the indirect measure of tracer in the duodenum, as calculated from Equations 3
and 4
.
 | (5) |
The passive fraction was also calculated as before but normalized using the direct measure of intraduodenal 3-O-[3H]methylglucose (MGD) and L-[14C]glucose (L-GLCD) radioactivity (Equation 6)
.
 | (6) |
The rates of transporter-mediated and passive absorption were calculated using Equations 7
and 8
, respectively.
 | (7) |
 | (8) |
The absorption of L-Glc before and during the phloridzin infusion, normalized for bolus radioactivities, was calculated using Equation 9
.
 | (9) |
The difference between portal venous and arterial [scap]l-GLC after the 80-min bolus was divided by four to account for the fourfold higher radioactivity in the second bolus.
Net hepatic glucose balance (NHGB) and fractional extraction (NHGFE) were calculated as previously described (11
).
Statistics.
All data presented herein are represented as the mean ± SEM ANOVA was performed to assess differences between calculation methods, absorption over time, and arterial plasma hormone concentrations. Paired t tests were used to determine differences between absorption with and without the intraduodenal phloridzin infusion. Differences were considered significant if P < 0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Arterial and portal vein blood glucose levels were 4.6 ± 0.1 and 4.3 ± 0.1 mmol/L, respectively, during the basal period. A sample could not be obtained from the duodenum during the basal period because the dogs were postabsorptive. During the intraduodenal glucose infusion, duodenal glucose levels were 210 ± 6 mmol/L (from t = 20 to 60 min), whereas arterial and portal vein levels rose to 6.3 ± 0.2 and 7.3 ± 0.3 mmol/L, respectively (Fig. 2a
). During the phloridzin infusion, arterial blood levels did not change significantly from the levels before the phloridzin infusion due to the isoglycemic clamp. Portal vein blood glucose fell significantly during the phloridzin infusion to 6.1 ± 0.1 mmol/L. Duodenal glucose was not significantly different during the phloridzin infusion. Intraduodenal radioactivities of both tracers reached peak values at t = 21 min (Fig. 2
b and c). Portal venous and arterial tracer concentrations rose steadily after the administration of the bolus and reached a plateau by t = 25 min. At the time of the second bolus injection (t = 80 min), tracer levels had fallen >100-fold. As with the first bolus injection, intraduodenal tracer concentrations peaked 1 min after injection (t = 81 min). Portal venous and arterial tracer concentrations, however, remained at levels measured before the administration of the second bolus.
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Insulin levels rose 2.5-fold with the administration of the intraduodenal glucose infusion and remained elevated during the phloridzin infusion and isoglycemic clamp (Table 1)
. Glucagon did not change significantly from basal levels during the intraduodenal glucose load or phloridzin infusion periods. Portal vein flow did not change significantly during the study. Glucose was infused peripherally to maintain isoglycemia during the phloridzin infusion. NHGB was 10.3 ± 1.5 µmol/(kg · min) (a positive number reflects net output) before the glucose infusion period. During the glucose infusion period, NHGB was -7.9 ± 2.4 µmol/(kg · min). NHGB during the phloridzin period [-3.3 ± 3.9 µmol/(kg · min)] did not differ significantly from values before its infusion. NHGFE during the glucose infusion was 0.04 ± 0.01 and did not change significantly during the phloridzin infusion (0.01 ± 0.02).
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On the basis of the appearance of tracers in the portal vein, passive gut glucose absorption was calculated to be 11 ± 2, 10 ± 2 and 9 ± 3% using Equations 2 , 5 and 6 , (i.e., transporter-mediated absorption was 89 ± 1, 90 ± 2 and 91 ± 2%). There were no significant differences among the calculation methods.
NGGO, net transporter-mediated and passive glucose absorption, and phloridzin-blocked glucose absorption.
Before the onset of the intraduodenal glucose, NGGO was slightly negative [-5.3 ± 0.6 µmol/(kg · min)] (Fig. 3
). During the intraduodenal glucose infusion, NGGO rose to 21.1 ± 3.0 µmol/(kg · min), with transporter-mediated and passive absorption calculated using Equations 7
and 8
equal to 18.5 ± 2.7 and 2.4 ± 0.04 µmol/(kg · min), respectively (Fig. 4
). The intraduodenal phloridzin infusion virtually abolished NGGO because rates were not significantly different than zero from t = 70 to 90 min. Phloridzin eliminated not only transporter-mediated glucose absorption, but also passive absorption. Because the absorption of L-Glc is relatively low, this variable was plotted on an amplified scale to highlight the effects of phloridzin (Fig. 5
). L-Glc absorption occurred after the administration of the t = 20 min bolus, but was abolished after administration of the bolus delivered at t = 80 in the presence of phloridzin.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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), but far less is understood about the mechanism of gut glucose absorption. Here we describe a method of assessing transporter-mediated and passive gut glucose absorption in the conscious state that can be applied to the study of nutritional, physiologic (e.g., exercise) and pathophysiologic (e.g., diabetes) conditions. With this technique, we demonstrate that in healthy dogs, all of the glucose absorbed from the gut is directly or indirectly dependent on transporter-mediated glucose absorption.
The experimental model uses arterial-venous and intraduodenal sampling techniques with isotopic tracer methods to assess gut glucose absorption. Due to uncertainties regarding bolus mixing, catheter position and intestinal transit time, the percentage contributions of transporter-mediated and passive gut glucose absorption were calculated using three different equations. To account for these difficulties, the passive fraction was determined using calculations that were both dependent and independent of direct intraduodenal sampling. Each calculation utilized the gut output of glucose analogs. We assumed in Equation 2
that the analog ratio in the duodenum is the same as that delivered to the gut in the bolus. The intraduodenal analog ratio was determined indirectly in Equation 5
by subtracting the rate of gut analog absorptions over time from the initial amount of analogue injected in the bolus. The analog ratio was determined by direct sampling of glucose analogue radioactivity in the gut lumen in Equation 6
. The calculations yielded results that were essentially the same, irrespective of whether the values were calculated using direct or indirect measures of isotope ratios in the duodenum. Because direct and indirect measurements gave the same results, it is likely that the ratio of glucose analog radioactivities obtained by intraduodenal sampling is representative of the ratio to which the luminal wall is exposed. Because MG is absorbed from the gut at a faster rate than L-Glc, accumulation of L-Glc in the gut, relative to MG, will occur with time, thus altering the ratio of the glucose analogs. Because calculation of the passive fraction from the ratio of glucose analog radioactivity in the bolus and the duodenal sample yields the same results, we conclude that there is not a large accumulation of L-Glc relative to MG during the 5-min period immediately after the bolus injection. It is important to recognize that in rats at least, transporter-mediated absorption predominates over a range of 5–400 mmol/L (13
).
To independently assess the functional role of gut transporter-mediated glucose absorption in contributing to the blood glucose pool, phloridzin was infused directly into the duodenum. Phloridzin is a potent inhibitor of the SGLT1 Na+/glucose cotransporter in the gut. Phloridzin inhibits the transport of Na+ across the luminal wall and by doing so inhibits the transporter-mediated absorption of glucose (14
). Due to the potential effects of glycemic level on NGGO (15
), an isoglycemic clamp was used to maintain arterial glucose concentrations during the phloridzin infusion at the levels seen during the previous period. During the phloridzin infusion, the glucose infusion rate required to maintain isoglycemia exceeded the rate of phloridzin-blocked glucose absorption. We speculate that the elevated glucose required to maintain isoglycemia is due to phloridzin entry into the bloodstream and subsequent exposure to the SGLT1 transporters at the kidney. This would inhibit glucose reabsorption into the circulation, increasing the exogenous glucose requirement.
The model described in the present paper is an adaptation of the model developed by Uhing and Kimura (6
) who used chronically catheterized rats. The methodology developed for rats relies on the rate of MG and L-Glc increase in the blood after administration of these isotopes in the gut to assess the fractions of transporter-mediated and passive gut glucose absorption. The model used in this paper directly assesses the rates of appearance of glucose and glucose analogs in the portal vein and can thereby quantify not only the passive and transporter-mediated fractions but also the absolute rates of absorption from the intestine. Another method using the dog model requires the separation of a section of the jejunum from the intestinal tract to form a closed loop for perfusion of substrates and markers (7
). Transporter-mediated and passive absorption is assessed using this technique by measuring the disappearance of glucose analogs from the perfused jejunal loop. This perfusion model is advantageous because it allows for the accurate assessment of jejunal volume. The separation of a section of the jejunum from the rest of the small intestine, however, could affect normal gut function. Additionally, the expression of glucose and fructose transporters has been shown to be highest in the duodenum with expression gradually decreasing down the length of the small intestine (16
). Thus, jejunal absorption may not be representative of absorption by the entire gut.
Recent studies in perfused rat jejunum have described a mechanism for gut glucose absorption that involves GLUT2-mediated facilitated diffusion (17
,18
). This mechanism of glucose transport is initiated by the active transport of glucose via SGLT1. Glucose absorption via this transporter stimulates the translocation of the GLUT2 facilitative transporter to the luminal surface of the gut. The method presented in this paper cannot discriminate between active and facilitated transport because MG is absorbed by both processes and L-Glc is absorbed by neither. However, it does allow for the separation of both of these processes from paracellular diffusion. The infusion of phloridzin blocks active transport; it would thereby prevent putative translocation of GLUT2 to the luminal wall and block both active and facilitative processes. Interestingly, our findings show that inhibition of transporter-mediated absorption with phloridzin impairs paracellular glucose absorption as well. This model fits with the concept of solvent drag in which transporter-mediated transport stimulates movement of glucose through gap junctions in the gut (4
,19
). However, this earlier work was performed in either anesthetized small animal models or in isolated perfused gut sections. The extension of this concept to the present study is important because research has shown that such manipulations can greatly increase passive gut glucose absorption.
In summary, a method is described that combines chronic catheterization of the gut and the blood vessels that perfuse and drain it with administration of isotopic glucose analogs to assess the contributions of transporter-mediated and passive processes to gut glucose absorption in a conscious large animal model. Most (90%) gut glucose absorption is transporter mediated. Administration of phloridzin, which directly inhibits SGLT1 glucose transport, completely abolished NGGO as an active and facilitated transport and as a passive transport as well. These findings demonstrate that in healthy dogs, all of the pathways of gut glucose absorption are either directly or indirectly dependent on active transport. The model system described here is applicable to assessing regulation of transporter-mediated and passive gut glucose absorption under a variety of conditions.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: A, artery; [A], arterial concentration; B, bolus; D, duodenal; GLUT, glucose transporter; I, indirect; ICG, indocyanine green; L-Glc, L-[14C]glucose; MG, 3-O-[3H]methylglucose; NGGO, net gut glucose output; NHGB, net hepatic glucose balance; NHGFE, net hepatic glucose fractional extraction; P, portal vein; [P], portal vein concentration; PVF, portal vein flow; SGLT1, Na+/K+ ATP-dependent transporter.
Manuscript received 18 January 2002. Initial review completed 4 February 2002. Revision accepted 13 March 2002.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1. Ferraris, R. P. & Diamond, J. (1997) Regulation of intestinal sugar transport. Physiol. Rev. 77:257-302.
2. Cheeseman, C. I. (1993) GLUT2 is the transporter for fructose across the rat intestinal basolateral membrane. Gastroenterology 105:1050-1056.[Medline]
3. Hediger, M. A., Coady, M. J., Ikeda, T. S. & Wright, E. M. (1987) Expression cloning and cDNA sequencing of the Na+/glucose co-transporter. Nature 330:379-381.[Medline]
4. Pappenheimer, J. R. & Reiss, K. Z. (1987) Contribution of solvent drag through intercellular junctions to absorption of nutrients by the small intestine of the rat. J. Membr. Biol. 100:123-136.[Medline]
5. Pappenheimer, J. R. (1988) Physiological regulation of epithelial junctions in intestinal epithelia. Acta Physiol. Scand. Suppl. 571:43-51.
6. Uhing, M. R. & Kimura, R. E. (1995) Active transport of 3-O-methyl-glucose by the small intestine in chronically catheterized rats. J. Clin. Investig. 95:2799-2805.
7. Lane, J. S., Whang, E. E., Rigberg, D. A., Hines, O. J., Kwan, D., Zinner, M. J., McFadden, D. W., Diamond, J. & Ashley, S. W. (1999) Paracellular glucose transport plays a minor role in the unanesthetized dog. Am. J. Physiol. 276:G789-G794.
8. Boyd, C. A. & Parsons, D. S. (1978) Effects of vascular perfusion on the accumulation, distribution and transfer of 3-O-methyl-D-glucose within and across the small intestine. J. Physiol. 274:17-36.
9. Boyd, C. A. & Parsons, D. S. (1979) Movements of monosaccharides between blood and tissues of vascularly perfused small intestine. J. Physiol. 287:371-391.
10. Hamilton, K. S., Gibbons, F. K., Bracy, D. P., Lacy, D. B., Cherrington, A. D. & Wasserman, D. H. (1996) Effect of prior exercise on the partitioning of an intestinal glucose load between splanchnic bed and skeletal muscle. J. Clin. Investig. 98:125-135.[Medline]
11. Galassetti, P., Shiota, M., Zinker, B., Wasserman, D. H. & Cherrington, A. D. (1998) A negative arterial portal vein glucose gradient decreases skeletal muscle glucose uptake in the conscious dog. Am. J. Physiol. 275:E101-E111.
12. Cherrington, A. D. (1999) Banting Lecture 1997. Control of glucose uptake and release by the liver in vivo. Diabetes 48:1198-1214.[Medline]
13. Uhing, M. R. & Kimura, R. E. (1995) The effect of surgical bowel manipulation and anesthesia on intestinal glucose absorption in rats. J. Clin. Invest. 95:2790-2798.
14. Oulianova, N., Falk, S. & Berteloot, A. (2001) Two-step mechanism of phlorizin binding to the SGLT1 protein in the kidney. J. Membr. Biol. 179:223-242.[Medline]
15. Schvarcz, E., Palmer, M., Aman, J., Horowitz, M., Stridsberg, M. & Berne, C. (1997) Physiological hyperglycemia slows gastric emptying in normal subjects and patients with insulin-dependent diabetes mellitus. Gastroenterology 113:60-66.[Medline]
16. Lenzen, S., Lortz, S. & Tiedge, M. (1996) Effect of metformin on SGLT1, GLUT2, and GLUT5 hexose transporter gene expression in small intestine from rats. Biochem. Pharmacol. 51:893-896.[Medline]
17. Kellett, G. L. & Helliwell, P. A. (2000) The diffusive component of intestinal glucose absorption is mediated by the glucose-induced recruitment of GLUT2 to the brush-border membrane. Biochem. J. 350:155-162.
18. Helliwell, P. A., Richardson, M., Affleck, J. & Kellett, G. L. (2000) Regulation of GLUT5, GLUT2 and intestinal brush-border fructose absorption by the extracellular signal-regulated kinase, p38 mitogen-activated kinase and phosphatidylinositol 3-kinase intracellular signalling pathways: implications for adaptation to diabetes. Biochem. J. 350:163-169.
19. Pappenheimer, J. R. & Volpp, K. (1992) Transmucosal impedance of small intestine: correlation with transport of sugars and amino acids. Am. J. Physiol. 263:C480-C493.
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Phloridzin infusion: 4 µmol/kg primed, 0.22 µmol/(kg · min) constant infusion. 
Variable glucose infusion into the vena cava.
), and portal vein (•) concentrations of glucose (a), MG (b) and L-Glc (c) during the delivery of an intraduodenal glucose load in conscious dogs. Arrows denote the time at which an intraduodenal tracer bolus was delivered. Data are means ± SEM, n = 6.
