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1 Department of Biology (Area 3), University of York, York YO10 5YW, UK
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(Received 2 August 2004;
accepted after revision 4 August 2004;
first published online 5 August 2004)
Corresponding author E. J. Shepherd: Department of Biology (Area 3), University of York, York YO10 5YW, UK. Email: ejs9{at}york.ac.uk
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Introduction |
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GLUT2 is a high capacity transporter, with a high Km, which displays a normal Michaelis-Menten type saturation response in basolateral membrane vesicles. However, the activation and rapid insertion of GLUT2 into the brush-border membrane results in a co-operative response by which absorptive capacity is matched precisely to dietary intake, so that GLUT2 affords the major route of absorption at high glucose concentrations (Kellett & Helliwell, 2000). In addition, and of equal importance, the intrinsic activity of GLUT2 is rapidly regulated over a 9-fold range in response to the same stimuli (Helliwell et al. 2000b). In this model, since GLUT2 transports not only glucose but also fructose (Cheeseman, 1993), it follows that fructose absorption across the brush-border membrane is mediated not only by GLUT5, which is highly specific for fructose, but also by GLUT2 (Helliwell et al. 2000a, 2000b; Au et al. 2002; Gouyon et al. 2003).
The GLUT2 component of intestinal glucose absorption has the potential to be regulated by hormones through the various intracellular signalling pathways. Until now, however, the only hormone identified as a regulator is glucagon-like peptide-2 (GLP-2; Au et al. 2002). In this paper, we now report that the GLUT2 component is regulated by glucocorticoids in response to stress stimuli. The stress response was caused by major building and renovation works in the expansion and modernization of the Department of Biology at York. Throughout the work there was no adverse effect on animal welfare and animals are now housed in a new, state-of-the-art animal facility. The first part of this paper therefore describes an opportunistic set of experiments in response to variable stress stimuli of ill-defined origin and character. The second part of the paper describes controlled experiments to support the conclusions drawn from the opportunistic experiments.
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Methods |
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All procedures used conformed to the UK Animals (Scientific Procedures) Act 1986. Male Wistar rats (240–270 g) were fed ad libitum on standard Bantin and Kingman rat and mouse diet with free access to water or saline solution as required.
As soon as we observed inhibition of the GLUT2 component of glucose absorption during the first phase of building works (see Results section), we informed the Animal House Manager and the Department's Home Office Liaison Officer. The in-house veterinary surgeon, the Department's Ethics Committee and the Home Office Inspector were also duly informed. Throughout the period of construction and modernization work, regular monitoring of animals by these authorities found that there was no discernible effect on animal welfare. There was no effect on frequency of breeding, feeding or drinking habits, cage behaviour, illness or disease, or in visual animal condition, such as coat appearance. Regular screens for viral and bacterial infection throughout the work were negative.
Drug treatments
Metyrapone. Rats were given 0.05% metyrapone (2-methyl-1,2-di-3-pyridyl-1-propane, Sigma Chemical Co.) in 0.9% NaCl as drinking water for a minimum of 72 h during stressful conditions prior to perfusion studies.
Dexamethasone. Control rats were given an intraperitoneal injection of 5.0 mg dexamethasone 21-sodium phosphate (Sigma Chemical Co.) per kilogram body weight in 0.9% NaCl approximately 60 min prior to perfusion studies. All perfusions using either metyrapone-treated rats or dexamethasone-injected rats were performed in conjunction with a control, i.e. a rat given 0.9% NaCl as a replacement for drinking water or as an I.P. injection was perfused simultaneously to confirm that either stressed or control conditions prevailed, where appropriate.
Perfusion of jejunal loops
Rats were anaesthetized by an I.P. injection of a mixture of 1.0 ml Hypnorm (Janssen Animal Health) and 0.5 ml Hypnovel (Roche Diagnostics) per kilogram body weight. Additional doses of 0.4 ml Hypnorm/0.2 ml Hypnovel per kilogram body weight were administered by an intramuscular route when required as determined by tail, foot and corneal reflexes, which were carefully monitored throughout the perfusion. Rats were humanely killed by exsanguination under anaesthetic at the end of the experiment. Jejunal loops were perfused luminally in vivo with 75 mM D-glucose in a modified Krebs-Henseleit buffer, pH 7.4, as previously described (Kellett & Helliwell, 2000). The perfusate also contained [3H]-inulin (Amersham International), a non-transportable marker, to permit the determination of water transport. Phloretin (1 mM; Sigma Chemical Co.), a specific inhibitor of GLUT2, was utilized to determine the relative contributions of SGLT1 and GLUT2 components in glucose absorption under different conditions. The perfusion consisted of a gas-segmented single pass system with perfusate and gas flow rates of 0.75 and 0.38 ml min–1, respectively, used to disrupt the unstirred layer. Luminal outflow was sampled every 5 min for a 1-min period, aliquots of which were analysed using a COBAS automatic analyser (Roche) for glucose concentration using a test kit (Trinder) obtained from Sigma Chemical Co. The concentration of glucose in the perfusate was calculated with correction for losses in perfusate volume caused by water transport. The rate of glucose transport, expressed as µmol min–1 (g dry weight)–1, was measured at the steady state period, achieved at t = 20 min.
Membrane vesicle preparation
Brush-border membrane vesicles were prepared as previously described (Corpe et al. 1996): every step of the procedure was performed at 0–4°C to prevent changes in trafficking after the intestine had been excised. Briefly, immediately following perfusion, the jejunum was flushed with ice-cold buffered mannitol (20 mM imidazole buffer, pH 7.5, containing 250 mM mannitol and 0.1 mM phenylmethane sulphonyl fluoride (PMSF)) in order to arrest potential trafficking of GLUT2. The jejunum was then placed on an ice-cold glass plate and slit longitudinally. Mucosal scrapings were taken with an ice-cold glass slide and homogenized immediately at 4°C in buffered mannitol using a Kinematica Polytron homogeniser (4 x 30 s bursts using the large probe at setting 7). The remainder of the preparation and its characterization for purity were as detailed by (Corpe et al. 1996).
SDS-PAGE analysis of membrane components
SDS-PAGE and Western blotting were performed as previously described using ECL (Enhanced Chemiluminescence) detection (Corpe et al. 1996; Helliwell et al. 2000a). All immmunoblotting was performed using rabbit polyclonal antibodies. For GLUT2, one was raised at York to 15 amino acids at the C-terminus (KATVQMEFLGSSETV), whereas the second was raised to a sequence contained in the large extracellular loop (SHYRHVLGVPLDDRRA) and was commissioned from Research Genetics, USA. An SGLT1 antibody, also from Research Genetics, was raised against the extracellular loop (RNSTEERIDLDA). For the detection of PKC ßII, a C18 antibody to the last 18 amino acids was purchased from Santa Cruz, CA, USA. Neutralization of all antibodies with the corresponding peptide (antibody to peptide 1: 1 v/v, peptide 50 µg ml–1) prior to blotting abolished labelling, confirming the specificity of the antibodies. Quantification of Western blots was performed using a Flowgen AlphaImager 1200 analysis system (Alpha Innotech Corporation, CA, USA). Relative protein levels detected in brush-border membranes under various conditions, as indicated by band intensities, were expressed with respect to preparations from control (unstressed) rats or stressed rats as appropriate. The same loading of 20 µg protein was used for all samples.
Statistical analysis
Values are presented as means ± S.E.M and were tested for significance using paired or unpaired Student's t test where appropriate.
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Results |
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The stress stimuli were ill-defined. Some were obvious to humans, such as intermittent audible noise. On other occasions vibrations were apparent as a direct result of work being carried out near the animal house. On many occasions when the system was not working, however, nothing could be readily identified as responsible for inhibition of the GLUT2 component of absorption. We were left to surmise that the rats were sensitive to noise frequencies and vibration levels not detectable by humans. Because of the nature of the work in different phases, the fact that it was a major building project and the relative inability to monitor the stress stimuli, all the experiments on stressed rats were opportunistic.
In control perfusions in unstressed rats in vivo with 75 mM glucose (Fig. 2, squares), the rate of glucose absorption reached a steady state rate at 15–20 min of 40.65 ± 2.9 µmol min–1 (g dry weight)–1 (mean ± S.E.M.). This was sustained for 75–90 min, although occasionally, as in Fig. 2, there was a slight tailing off towards the end. Work on the new building commenced with pile driving and steel construction. During this initial phase, we observed for the first time that the rate of glucose absorption was not adequately sustained throughout the full period of the perfusion (Fig. 2, circles). With 75 mM glucose perfused through the lumen, rates peaked at 15 min at a value not significantly different from that of control perfusions. However, the rate of absorption after 25 min began to fall and continued to do so. When heavy construction work ceased, perfusions returned rapidly to control properties and a large, strongly regulated GLUT2 component of absorption operated perfectly until the renovation and modernization of the old building began.
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Since metyrapone inhibits 11-ß-hydroxylase, we investigated the effect of a poorly metabolized analogue of cortisol, the synthetic glucocorticoid, dexamethasone 21-sodium phosphate. Dexamethasone was injected intraperitoneally into control rats; these were subsequently demonstrated to be initially stress-free by simultaneous injection of a rat with saline only. These corresponding controls show a rate of 37.17 ± 1.64 µmol min–1 (g dry weight)–1 (n = 5) confirming that no stress response to building work was present throughout these experiments. Table 1 shows that injection of dexamethasone 60 min prior to perfusion resulted in a reduction in the GLUT2 component of absorption of 71.4 ± 3.9% (P < 0.0001 and P = 0.27 for comparison with control and stressed rats, respectively). There was no effect of dexamethasone on glucose absorption in stressed rats, i.e. the effects were not additive (28.73 ± 1.84 µmol min–1 (g dry weight)–1 (n = 4), P = 0.1 compared with stressed rats not injected with dexamethasone). Again, simultaneous perfusions in rats injected with saline only confirmed that stress conditions prevailed (23.69 ± 1.15 µmol min–1 (g dry weight)–1 (n = 3)). The reduction in absorption observed in dexamethasone-injected control rats was accompanied by a 49.2 ± 8.2% and 46.0 ± 14.3% reduction in the level of GLUT2, detected by C-terminus and extracellular loop antibodies (P < 0.01 and P < 0.05, respectively; Fig. 4). SGLT1 was not affected (–5.4 ± 2.8%, P = 0.21 compared with control rats).
In a parallel project during renovation of wing F, rats deprived of food overnight (18 h-starved) were also perfused on days when fed rats were stressed and glucose absorption was strongly inhibited. Of particular interest, the absorption of glucose in 18 h-starved rats was unaffected by stress: the control rate of absorption for starved rats was 48.61 ± 1.1 µmol min–1 (g dry weight)–1 (n = 4) and the rate for starved rats under proven stress conditions (as indicated by the rate of absorption in fed rats) was 39.72 ± 0.8 µmol min–1 (g dry weight)–1 (n = 4) (P = 0.14).
Table 1 shows the effects of stress stimuli and dexamethasone injection on the absorption of water by the jejunum during the perfusions, as measured by the non-transportable marker [3H]-inulin. A 17.6 ± 2.6% reduction in the mean value of water absorption in perfusions with stressed rats was not statistically significant compared with control perfusions (P = 0.34). However, dexamethasone injection into control rats caused a severe 58.8 ± 2.4% inhibition in water absorption (P < 0.001). Metyrapone administration caused a 28.6 ± 1.8% increase in water absorption in stressed rats (P < 0.05), although there was no difference when compared with control values (P = 0.53).
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Discussion |
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During renovation work, when the effects were more intense, glucose absorption was inhibited 36.4 ± 3.0%; moreover, absorption was inhibited as soon as the steady state was achieved. Use of phloretin to inhibit the GLUT2 component selectively in whole intestine in stressed and control rats revealed that stress caused a 42.8 ± 3.8% inhibition of the GLUT2 component (Table 1): there was a concomitant diminution of 66.0 ± 15.9 and 66.3 ± 5.6% in the level of GLUT2, when determined with the C-terminal and the extracellular loop antibody, respectively (Fig. 4). There was no significant effect of stress on the SGLT1 component of absorption or on the level of SGLT1 protein (Table 1, Fig. 4). The effect of stress was relatively rapid, as shown on days 58 and 59 in Fig. 2, when work on the animal house roof was undertaken.
Three observations implicate the glucocorticoid cortisol as the most likely hormone involved in the inhibition of glucose absorption in stressed rats. First, the administration of metyrapone in the drinking water reversed the effects of stress; metyrapone inhibits 11-ß-hydroxylase to maintain plasma cortisol at basal levels. Metyrapone has also been shown to cause an increase in noradrenaline and dopamine production (Bratt et al. 2001; Laborie et al. 2003); however, the fact that metyrapone has no effect on glucose absorption in control animals excludes a role of these hormones and adrenaline in the stress response, a conclusion supported by our observation that H89 fails to reverse the effects of stress, thus ruling out the major alternative stress signals to cortisol. Second, injection of the poorly metabolized synthetic analogue of cortisol, dexamethasone-21-phosphate, into control rats 60 min before perfusion strongly inhibited the GLUT2 component of glucose absorption (Table 1). The GLUT2 component is inhibited to a slightly greater extent by dexamethasone than that observed in the stress response from building works. The differences in the two situations may simply be due to the fact that dexamethasone is 30 times more potent than cortisol (Quaroni et al. 1999). Third, dexamethasone treatment of control rats diminished the level of GLUT2 but increased the level of PKC ßII by approximately 48 and 58.5%, respectively, a response very similar to that observed in stressed rats (Figs 4 and 5). This observation was unexpected, since increased apical GLUT2 insertion correlated with increased PKC activation in all previous investigations. Ideally, we would like to have measured changes in circulating levels of cortisol in stressed rats; however, this opportunity was lost because of the opportunistic nature of our experiments on the stress response.
Inhibition of glucose absorption by stress and dexamethasone therefore results from inhibition of GLUT2 trafficking. Trafficking is a rapid process with a half-time of the order of 3 min (Kellett & Helliwell, 2000). Cortisol has a half-life of 30–60 min in vivo and stress causes an increase in its synthesis coupled with an increase in its half-life in the circulation (Herman et al. 1992; Calvo & Volosin, 2001). The effects of stress were rapid and dexamethasone exerted full inhibition of absorption within 60 min. The rapidity of the glucocorticoid response most probably represents a non-genomic, direct effect on the trafficking mechanism. The GLUT2 system shows significant similarities to the inhibition of insulin-induced 2-deoxyglucose uptake through GLUT4 by treatment of adipocytes or soleus muscle for 60 min with dexamethasone: in both adipocytes and soleus muscle, dexamethasone causes translocation of PKC to the plasma membrane and in adipocytes the isoform involved is PKC ß (Ishizuka et al. 1995; Kajita et al. 2001). Moreover, chronic administration of dexamethasone inhibits rapid trafficking of GLUT4 to the membrane of rat soleus muscle without altering the cellular content of GLUT4, thereby inducing insulin resistance (Dimitriadis et al. 1997). The fact that PKC ßII is activated but apical GLUT2 levels are diminished in response to stress or dexamethasone suggests that glucocorticoid inhibits GLUT2 insertion by a parallel pathway acting downstream of PKC ßII activation. The possibility of such a pathway deserves detailed investigation. Prolonged administration of dexamethasone had no effect on glucose uptake as measured by in vitro methods, in which transport was mediated exclusively by SGLT1 at the brush-border membrane (Thiesen et al. 2003a, b). In addition, protein and mRNA levels of SGLT1 remain unchanged. These data agree with the present short-term regulation studies implicating inhibition of GLUT2 trafficking as the mechanism of inhibition of glucose absorption by glucocorticoids.
An inhibitory effect of dexamethasone on jejunal water absorption was evident from the perfusions. Thus a 71.4 ± 3.9% inhibition of the GLUT2 component of glucose absorption was accompanied by a 58.8 ± 2.4% inhibition of water absorption (Table 1). However, in stressed animals, there was no significant inhibition of water absorption, despite a similar inhibition of the GLUT2 component. This may also be attributed to the potency of dexamethasone. Nevertheless, there is a clear dissociation between water and glucose absorption. Such dissociation is not consistent with the proposal that glucose absorption at concentrations above those required to saturate SGLT1 is the result of paracellular flow (Pappenheimer & Reiss, 1987). Gruzdkov and colleagues have recently provided a definitive demonstration that water transport and glucose absorption can be dissociated. Accordingly, by manipulating the osmolarity of the perfusion medium at high glucose concentrations, Gromova et al. (2001) have shown that very high rates of glucose absorption can occur not only in the presence of water absorption, but also in the face of water secretion. Moreover, we have previously reported that simultaneous inhibition of the GLUT2 and SGLT1 components can account for within experimental error for all glucose absorption (Helliwell & Kellett, 2002).
Stress and gastrointestinal function
Stress has been frequently associated with gastrointestinal manifestations, for example, changes in gastric emptying, increased colonic and small intestinal motility, and intestinal barrier function (Bijlsma et al. 2001). A variety of clinical evidence demonstrates a relationship between stress and specific gastrointestinal functions, thought to be mediated by neural pathways linking the CNS and the gut (summarized in Saunders et al. 1994).
An elevated plasma cortisol concentration is recognized as a classic response to stress (Saunders et al. 1994; Calvo et al. 1998). The initial response of individuals or animals to stress is activation of the sympathetic nervous system followed by rapid secretion of adrenaline by the adrenal medulla. The resulting fright, fight or flight response includes enhanced mobilization of glucose and fat and redistribution of blood flow from the skin and gut to the brain and muscle. However, the adrenal medulla releases only minute amounts of material and so response to prolonged stress is taken over by sustained secretion of cortisol in response to activation of the HPA axis. Thus cortisol secretion from the adrenal cortex is stimulated by rapid secretion of adrenocorticotrophic hormone (ACTH) from the anterior pituitary, which in turn is caused by the secretion of corticotrophin releasing hormone (CRF) from the hypothalamus (DeRijk et al. 2002). Access to dietary glucose is a pre-requisite for HPA stress responses. Thus, in humans fasted for 8–11 h before being subjected to a controlled stress test, there was a doubling in plasma cortisol levels within 15 min, provided that the subjects received a 100 g glucose load 1 h before the test: if, instead of glucose, they received either tap water or a protein or a fat load, there was no increase in plasma cortisol levels above basal (Kirschbaum et al. 1997; Gonzalez-Bono et al. 2002). Consistent with these findings, we observed during the renovation of wing F that stress had no effect on the rate of glucose absorption in rats from which food was withheld overnight.
Animal welfare studies on the transport of piglets have revealed that stress induced by vibration causes an increase in plasma cortisol levels (Perremans et al. 2001). At times there was undoubtedly detectable vibration of the old animal house in wing E as a result of the renovation work in wing F and the effects of stress were blocked by metyrapone. Vibration therefore seems likely to have been a significant factor in the stress response of rats; indeed, it has long been known that rats are very much more sensitive to vibration than humans.
Why should cortisol inhibit the GLUT2 component of intestinal glucose absorption? As noted earlier, cortisol antagonizes the actions of insulin. At physiological concentrations, cortisol mobilizes energy stores in the periphery, stimulating glycogenolysis and lipolysis. Cortisol also inhibits protein synthesis, resulting in release of amino acids and loss of skeletal mass. The degradation products, lactate, glycerol and amino acids, are recovered by enhanced gluconeogenesis, assisted by stimulation of amino acid uptake in liver. In the periphery, cortisol inhibits both amino acid and glucose uptake, preventing potential inhibition of the mobilization process. After a meal high in free sugars or complex carbohydrate of high glycaemic index, the major route of transintestinal delivery of glucose into the circulation is mediated by GLUT2 in the brush-border membrane. The resulting increase in blood glucose levels would stimulate peripheral glucose uptake and restrict gluconeogenesis. The ability of cortisol to inhibit GLUT2 trafficking and absorption therefore seems necessary to prevent enhanced intestinal delivery of glucose from antagonizing the ability of cortisol to mobilize peripheral energy stores in response to prolonged stress. Our opportunistic experiments have afforded what is perhaps a unique demonstration that the possibility of such a mechanism is not just a deduction from a laboratory experiment; it operates in a real-life physiological situation.
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) control rats under stress-free conditions, no building work (n = 4); (•) rats during construction of the new building (n = 11); (
) rats during a period of intense renovation of wing F in the old building (n = 8).
