Jejunal Glucose Uptake Research Articles

Selection for Growth Does Not Affect Apparent Energetic Efficiency of Jejunal Glucose Uptake in Mice

Five-wk-old male mice from high growth (M16) and randomly bred control (ICR) lines, plus their reciprocal crosses, ICR × M16 and M16 × ICR, were used to investigate whether whole-body O2 consumption, jejunal respiration, jejunal glucose absorption and the apparent energetic efficiency of jejunal active glucose uptake in mice are altered by genetic selection for growth as well as by heterosis and maternal effects. Whole-body O2 consumption was measured in 12 mice from each line or cross. The mice were later killed for measurement of jejunal O2, using tissue respiration chambers and jejunal glucose transport determined by 3H-3-O-methylglucose accumulation. No heterosis or maternal effects were detected in jejunal glucose active transport and active glucose uptake. Selection for growth (M16 vs. ICR) increased daily gain (1.54 vs. 1.09 g, P < 0.001), small intestinal length and weight, but did not enhance jejunal glucose transport. The apparent energetic efficiency of jejunal active glucose uptake among lines was not different (54.0, 50.4, 51.6 and 47.1 nmol ATP expended/nmol glucose uptake for M16, ICR, M16 × ICR and ICR × M16, respectively, P > 0.63). Selection for growth in mice did not result in more energetically efficient jejunal glucose absorption.

Selection for Body Composition Does Not Affect Energetic Efficiency of Jejunal Glucose Uptake in Mice

Five-wk-old male mice from three lines were used to examine whether the apparent energetic efficiency of active jejunal glucose uptake in mouse jejunum is altered by genetic selection for different body composition. The mice lines were selected as follows: HE, high percentage of body fat with no change in body weight as a constraint; LF, low percentage of body fat; and RS, randomly bred control. Body weight was similar in all lines. Total jejunal O2 consumption and ouabain-sensitive O2 consumption were used to estimate the energy expenditure associated with glucose absorption and Na+/K+-ATPase activity. Tritiated 3-O-methyl-D-glucose was used to determine glucose uptake by mouse jejunum. Line LF, when compared with line HE, had lower body fat as indicated by epididymal fat pad weight (143 vs. 362 mg/mouse, P < 0.001). There were no significant differences in small intestinal weight, length and density (mg/cm) between LF and HE lines. Jejunal villus width was greater in line LF compared with line HE (115 vs. 92 µm, P < 0.002). Jejunal glucose transport and O2 consumption were not different between LF and HE lines. Ouabain-sensitive O2 consumption was not significantly different among the three lines. No differences were noted in the apparent energetic efficiency of active glucose uptake among lines.

Increased jejunal glucose uptake by 18F-FDG PET/CT with remission of type 2 diabetes after bariatric surgery

Increased jejunal glucose uptake by 18F-FDG PET/CT with remission of type 2 diabetes after bariatric surgery

Active transport of glucose across the jejunal epithelium decreases with age in broiler chickens

Intestinal glucose absorption varies with growth; however, the dynamics of these variations has not been yet fully elucidated in broiler chickens. The present study aimed to compare jejunal glucose uptake and maltose digestion in broilers of 2 different ages, i.e., 1- vs. 5 wk old. Oral D-maltose gavage, everted sac, and Ussing chamber experiments were carried out to investigate intestinal glucose absorption and mRNA expression of glucose-transport-related genes as well as jejunal maltase activity. Upon gavage, glucose concentrations peaked at 10min post-administration in 1-wk-old chicks, while they peaked at 40min in 5-wk-old chickens. Glucose concentrations at 10min were significantly higher in the 1-wk-old chicks (P = 0.010). Using the everted sacs experimental setup, 5 intestinal regions i.e., duodenum, proximal jejunum, distal jejunum, proximal ileum, and distal ileum, were targeted to examine D-maltose digestion and glucose transport across the intestinal mucosa. In the distal and proximal ileum, glucose concentrations were found to be significantly higher in the serosal compartment of the 1-wk-old chicks upon incubation with D-maltose (25mM) (P < 0.05), while in the mucosal compartment the levels were significantly higher in the 5-wk-old chickens (P < 0.05). An Ussing chamber setup was employed to measure glucose-induced short-circuit current (ΔIsc) in the mucosal epithelium of the jejunum. In response to the addition of D-maltose (10mM) into the mucosal compartment, ΔIsc was significantly higher in the 1-wk-old chicks (P = 0.018). Furthermore, no variations in jejunal maltase activity were observed between the 2 age groups. While jejunal glucose absorption was lower in the 5-wk-old chickens, the mRNA expression levels of jejunal SGLT1, GLUT2, and Na+/K+-ATPase did not show any significant differences between the 2 age groups. Our results suggest that the active transport of glucose across the jejunal epithelium decreases upon growth in broiler chickens but is not accompanied by any variations in maltase activity or in the expression of glucose-absorption-related genes.

Boerhaavia diffusa inhibits key enzymes linked to type 2 diabetes in vitro and in silico; and modulates abdominal glucose absorption and muscle glucose uptake ex vivo

The present study investigated the in vitro and ex vivo antioxidant, anti-diabetic and anti-obesogenic potentials of different solvent (ethyl acetate, ethanol and water) extracts from the aerial parts of Boerhaavia diffusa. The ferric reducing antioxidant power (FRAP), DPPH scavenging activity and the ameliorative effects of the extracts on Fe2+-induced oxidative injury was investigated both in vitro and ex vivo. Alpha glucosidase and pancreatic lipase inhibitory potentials of the extracts were examined in vitro, while the effects of the ethanol extract on abdominal glucose intake and muscle glucose uptake were determined in freshly harvested tissues ex vivo. The extracts were subjected to Gas Chromatography-Mass Spectrometry (GC–MS) analysis to identify their possible bioactive components. The ethanol extract showed the most potent FRAP and DPPH radical scavenging activities compared to other extracts. All extracts increased catalase and SOD activities, and GSH levels in oxidative pancreatic injury. Both ethanol and aqueous extracts exhibited remarkable enzyme inhibitory activities, which was significantly higher than ethyl acetate extract and acarbose but was not comparable to orlistat. The ethanol extract portrayed a dose-dependent inhibitory effect on jejunal glucose uptake and enhancement of muscle glucose uptake. 9-(4 methoxyphenyl) xanthene, xanthone and stigmasterol showed strong binding affinities for α-glucosidase and lipase enzymes tested. Data from this study suggest that aerial parts of B. diffusa (particularly the ethanol extract) may not only exhibit antioxidant potentials but may also mediate anti-lipidemic and anti-hyperglycemic effects via inhibiting fat and carbohydrate digestion as well as abdominal glucose intake and enhancing muscle glucose uptake.

Colectomy induces an aldosterone-mediated increase in jejunal glucose uptake in rats

AimsThe main function of the colon is water and electrolyte absorption. Total colectomy eliminates this colonic function and may alter the absorptive capacity of the small intestine for nutrients. This study examines the effect of total colectomy on jejunal glucose absorption and investigates the potential role of aldosterone in mediating the alterations in glucose uptake post-colectomy using the aldosterone antagonist spironolactone. Main methodsTotal colectomy with ileo-rectal anastomosis was performed on anesthetized rats. Sham rats were identically handled without colon resection. Two days post-surgery, groups of colectomized rats were injected with either a daily subcutaneous dose of spironolactone or sesame oil for 12days. Body weight changes and food and water intake were measured in all experimental groups. Glucose absorption was measured by in-vivo single pass perfusion in the rat jejunum of control, sham, colectomized, colectomized with spironolactone, and colectomized with sesame oil treatment. Na/K ATPase, SGK1, SGLT1 and GLUT2 expressions were determined in jejunal mucosa in control, colectomized and colectomized/spironolactone injected rats by Western blot analysis. Histological assessment was performed on jejunal sections in control and colectomized groups. Key findingsGlucose absorption significantly increased in colectomized rats with an observed increase in Na/K ATPase and SGK1 expression. No significant expression change in SGLT1 and GLUT2 was detected in the jejunum in colectomized rats. Spironolactone, however, significantly decreased the glucose uptake post-colectomy and normalized Na/K ATPase and SGK1 expression. SignificanceOur results suggest that jejunal glucose uptake increases post-colectomy as a possible consequence of an aldosterone-mediated function.

Gastrointestinal transport of calcium and glucose in lactating ewes.

During lactation, mineral and nutrient requirements increase dramatically, particularly those for Ca and glucose. In contrast to monogastric species, in ruminants, it is rather unclear to which extend this physiological change due to increased demand for milk production is accompanied by functional adaptations of the gastrointestinal tract (GIT). Therefore, we investigated potential modulations of Ca and glucose transport mechanisms in the GIT of lactating and dried‐off sheep. Ussing‐chamber technique was applied to determine the ruminal and jejunal Ca flux rates. In the jejunum, electrophysiological properties in response to glucose were recorded. Jejunal brush‐border membrane vesicles (BBMV) served to characterize glucose uptake via sodium‐linked glucose transporter 1 (SGLT1), and RNA and protein expression levels of Ca and glucose transporting systems were determined. Ruminal Ca flux rate data showed a trend for higher absorption in lactating sheep. In the jejunum, small Ca absorption could only be observed in lactating ewes. From the results, it may be assumed that lactating ewes compensate for the Ca loss by increasing bone mobilization rather than by increasing supply through absorption from the GIT. Presence of SGLT1 in the jejunum of both groups was shown by RNA and protein identification, but glucose uptake into BBMV could only be detected in lactating sheep. This, however, could not be attributed to electrogenic glucose absorption in lactating sheep under Ussing‐chamber conditions, providing evidence that changes in jejunal glucose uptake may include additional factors, that is, posttranslational modifications such as phosphorylation.

Anti-hyperglycemic Effect of the Aqueous Extract of Banana Infructescence Stalks in Streptozotocin-induced Diabetic Rats

Water extract of banana (Musa sapientum) infructescence stalks has been used in folk medicine in the treatment of diabetes mellitus. This work aims at verifying the claimed effect and elucidating its possible mode of action. The extract was given in replacement of drinking water to diabetic rats, and its mechanism of action was studied by investigating its involvement in glucose transport in Caco-2 monolayers, and in rat jejuna using an in situ perfusion technique. Its effect on the Na(+)/K(+) ATPase was studied by measuring the amount of inorganic phosphate liberated. The extract reduced significantly blood glucose levels in diabetic rats and glucose transport across rat jejuna and Caco-2 monolayers, and induced a 50% decrease in their Na(+)/K(+) ATPase activity. The extract did not induce any further decrease in jejunal glucose uptake in the simultaneous presence of phloridzin and phloretin, respective inhibitors of SGLT1 and GLUT2 transporters nor did it induce a change in the protein expression of SGLT1 and GLUT2. It was concluded that the extract acts by reducing the Na(+)/K(+) ATPase activity of enterocytes and consequently the sodium gradient required for sugar transport by SGLT1, which leads to down-regulation of GLUT2 and contributes to the observed anti-hyperglycemic effect.

Characterization of d-Glucose Transport across Equine Jejunal Brush Border Membrane Using the Pig as an Efficient Model of Jejunal Glucose Uptake

To test the hypotheses that glucose transport capacity across the brush border membrane (BBM) of the large colon is lower than that of the small intestine in equids, and that small intestinal transport capacity in equids is lower than suids. d-glucose transport capacity (Vmax) and affinity (KM) across the BBM of the distal jejunum (DJ) and proximal large colon (PLC) of the pony and pig were measured. Mucosa was collected from the DJ and PLC of ponies (n = 4) and pigs (n = 3), flash-frozen in liquid nitrogen, and stored at −80°C. Jejunal and colonic BBM vesicles were manufactured, and d-glucose transport was determined. There was no detectable active uptake of glucose in the equine PLC. Compared with the pig DJ, d-glucose transport capacity was lower (2595 ± 331 vs. 655 ± 286 ρmol·mg protein−1·s−1, respectively, P < .01) and transport affinity tended to be lower (0.09 ± 0.07 vs. 0.27 ± 0.06 mM, respectively, P = .11) in the pony DJ. Compared with the pig DJ, d-glucose transport capacity (2,595 ± 331 vs. 571 ± 331 ρmol·mg protein−1·s−1, respectively, P < .001) and transport affinity (0.09 ± 0.07 vs. 0.54 ± 0.07 mM, respectively, P < .001) in the pig PLC were lower. Results show there is negligible d-glucose uptake across pony PLC, and capacity for d-glucose absorption across DJ BBM is fourfold lower in the pony compared with the pig. Results further exemplify, at a physiological level, the limited capacity of the equid small intestine to transport glucose relative to an omnivorous mammal, and the likely evolutionary adaptation of equids to low dietary levels of nonstructural carbohydrates.

Upregulation of ACE2-ANG-(1–7)-Mas axis in jejunal enterocytes of type 1 diabetic rats: implications for glucose transport

The inhibitory effects of the angiotensin-converting enzyme (ACE)-ANG II-angiotensin type 1 (AT₁) receptor axis on jejunal glucose uptake and the reduced expression of this system in type 1 diabetes mellitus (T1DM) have been documented previously. The ACE2-ANG-(1-7)-Mas receptor axis is thought to oppose the actions of the ACE-ANG II-AT₁ receptor axis in heart, liver, and kidney. However, the possible involvement of the ACE2-ANG-(1-7)-Mas receptor system on enhanced jejunal glucose transport in T1DM has yet to be determined. Rat everted jejunum and Caco-2 cells were used to determine the effects of ANG-(1-7) on glucose uptake and to study the ACE2-ANG-(1-7)-Mas receptor signaling pathway. Expression of target gene and protein in jejunal enterocytes and human Caco-2 cells were quantified using real-time PCR and Western blotting. T1DM increased jejunal protein and mRNA expression of ACE2 (by 59 and 173%, respectively) and Mas receptor (by 55 and 100%, respectively) in jejunum. One millimolar ANG-(1-7) reduced glucose uptake in jejunum and Caco-2 cells by 30.6 and 30.3%, respectively, effects that were abolished following addition of 1 μM A-779 (a Mas receptor blocker) or 1 μM GF-109203X (protein kinase C inhibitor) to incubation buffer for jejunum or Caco-2 cells, respectively. Finally, intravenous treatment of animals with ANG-(1-7) significantly improved oral glucose tolerance in T1DM but not control animals. In conclusion, enhanced activity of the ACE2-ANG-(1-7)-Mas receptor axis in jejunal enterocytes is likely to moderate the T1DM-induced increase in jejunal glucose uptake resulting from downregulation of the ACE-ANG II-AT₁ receptor axis. Therefore, altered activity of both ACE and ACE2 systems during diabetes will determine the overall rate of glucose transport across the jejunal epithelium.

Jejunal nutrient sensing is required for duodenal-jejunal bypass surgery to rapidly lower glucose concentrations in uncontrolled diabetes

Gastrointestinal bypass surgeries restore metabolic homeostasis in patients with type 2 diabetes and obesity(1), but the underlying mechanisms remain elusive. Duodenal-jejunal bypass surgery (DJB), an experimental surgical technique that excludes the duodenum and proximal jejunum from nutrient transit(1,2), lowers glucose concentrations in nonobese type 2 diabetic rats(2–5). Given that DJB redirects and enhances nutrient flow into the jejunum and that jejunal nutrient sensing affects feeding(6,7), the repositioned jejunum after DJB represents a junction at which nutrients could regulate glucose homeostasis. Here we found that intrajejunal nutrient administration lowered endogenous glucose production in normal rats through a gut-brain-liver network in the presence of basal plasma insulin concentrations. Inhibition of jejunal glucose uptake or formation of long chain fatty acyl-coA negated the metabolic effects of glucose or lipid, respectively, in normal rats, and altered the rapid (2 d) glucose-lowering effect induced by DJB in streptozotocin (STZ)-induced uncontrolled diabetic rats during refeeding. Lastly, in insulin-deficient autoimmune type 1 diabetic rats and STZ-induced diabetic rats, DJB lowered glucose concentrations in 2 d independently of changes in plasma insulin concentrations, food intake and body weight. These data unveil a glucoregulatory role of jejunal nutrient sensing and its relevance in the early improvement of glycemic control after DJB in rat models of uncontrolled diabetes.

Characterization of D-Glucose Transport across Equine Jejunal Brush Border Membrane Using the Pig as an Efficient Model of Jejunal Glucose Uptake

Characterization of D-Glucose Transport across Equine Jejunal Brush Border Membrane Using the Pig as an Efficient Model of Jejunal Glucose Uptake

Diabetes mellitus and expression of the enterocyte renin-angiotensin system: implications for control of glucose transport across the brush border membrane

Streptozotocin-induced (Type 1) diabetes mellitus (T1DM) in rats promotes jejunal glucose transport, but the trigger for this response remains unclear. Our recent work using euglycemic rats has implicated the enterocyte renin-angiotensin system (RAS) in control of sodium-dependent glucose transporter (SGLT1)-mediated glucose uptake across the jejunal brush border membrane (BBM). The aim of the present study was to examine whether expression of enterocyte RAS components is influenced by T1DM. The effects of mucosal addition of angiotensin II (AII) on [(14)C]-D-glucose uptake by everted diabetic jejunum was also determined. Two-week diabetes caused a fivefold increase in blood glucose level and reduced mRNA and protein expression of AII type 1 (AT(1)) and AT(2) receptors and angiotensin-converting enzyme in isolated jejunal enterocytes. Angiotensinogen expression was, however, stimulated by diabetes while renin was not detected in either control or diabetic enterocytes. Diabetes stimulated glucose uptake into everted jejunum by 58% and increased the BBM expression of SGLT1 and facilitated glucose transporter 2 (GLUT2) proteins, determined by Western blotting by 25% and 135%, respectively. Immunohistochemistry confirmed an enhanced BBM expression of GLUT2 in diabetes and also showed that this was due to translocation of the transporter from the basolateral membrane to BBM. AII (5 microM) or L-162313 (1 microM), a nonpeptide AII analog, decreased glucose uptake by 18% and 24%, respectively, in diabetic jejunum. This inhibitory action was fully accountable by an action on SGLT1-mediated transport and was abolished by the AT(1) receptor antagonist losartan (1 microM). The decreased inhibitory action of AII on in vitro jejunal glucose uptake in diabetes compared with that noted previously in jejunum from normal animals is likely to be due to reduced RAS expression in diabetic enterocytes, together with a disproportionate increase in GLUT2, compared with SGLT1 expression at the BBM.

Resistin-Like Molecule-β Inhibits SGLT-1 Activity and Enhances GLUT2-Dependent Jejunal Glucose Transport

OBJECTIVEAn increased expression of RELM-β (resistin-like molecule-β), a gut-derived hormone, is observed in animal models of insulin resistance/obesity and intestinal inflammation. Intestinal sugar absorption is modulated by dietary environment and hormones/cytokines. The aim of this study was to investigate the effect of RELM-β on intestinal glucose absorption.RESEARCH DESIGN AND METHODSOral glucose tolerance test was performed in mice and rats in the presence and the absence of RELM-β. The RELM-β action on glucose transport in rat jejunal sacs, everted rings, and mucosal strips was explored as well as downstream kinases modulating SGLT-1 and GLUT2 glucose transporters.RESULTSOral glucose tolerance test carried out in rodents showed that oral administration of RELM-β increased glycemia. Studies in rat jejunal tissue indicated that mucosal RELM-β promoted absorption of glucose from the gut lumen. RELM-β had no effect on paracellular mannitol transport, suggesting a transporter-mediated transcellular mechanism. In studies with jejunal mucosa mounted in Ussing chamber, luminal RELM-β inhibited SGLT-1 activity in line with a diminished SGLT-1 abundance in brush border membranes (BBMs). Further, the potentiating effect of RELM-β on jejunal glucose uptake was associated with an increased abundance of GLUT2 at BBMs. The effects of RELM-β were associated with an increased amount of protein kinase C βII in BBMs and an increased phosphorylation of AMP-activated protein kinase (AMPK).CONCLUSIONSThe regulation of SGLT-1 and GLUT2 by RELM-β expands the role of gut hormones in short-term AMPK/protein kinase C mediated control of energy balance.

Dexamethasone and GLP‐2 Given to Lactating Rat Dams Influence Glucose Uptake in Suckling and Postweanling Offspring

Glucagon-like peptide-2 (GLP-2) enhances intestinal absorption in adult animals. Glucocorticosteroids accelerate the ontogeny of the intestine and increase sugar uptake in adult animals. Modifying the maternal diet during lactation alters nutrient uptake in the offspring. The authors hypothesized that GLP-2 and dexamethasone, when administrated to lactating rat dams, enhance sugar uptake in the suckling and postweanling offspring. Rat dams were treated during lactation with GLP-2 (0.1 microg/g/day subcutaneously [SC], twice daily), dexamethasone (0.128 microg/g/day SC, once daily), GLP-2 + dexamethasone (same doses), or placebo. The suckling offspring were sacrificed at 19-21 days of age, and the postweanlings were sacrificed 4 weeks later. Intestinal glucose and fructose uptake was assessed using an in vitro ring technique. GLP-2 and dexamethasone resulted in lower body weights, and dexamethasone caused intestinal atrophy in sucklings. The jejunal atrophy in sucklings given dexamethasone was prevented by GLP-2 + dexamethasone. In sucklings, the maximal transport rate and the Michaelis affinity constant for ileal glucose uptake were both increased by GLP-2 and GLP-2 + dexamethasone. In contrast, in postweanlings, the maximal transport rate for jejunal glucose uptake was reduced by dexamethasone and GLP-2, as was ileal fructose uptake. Treating lactating rat dams with GLP-2 or dexamethasone enhances glucose uptake in sucklings, but the late effect is a reduction in glucose and fructose absorption in postweanlings. The nutritional significance of these findings remains to be established.

Maternal dexamethasone and GLP-2 have early effects on intestinal sugar transport in their suckling rat offspring

Both glucagon-like peptide 2 (GLP-2) and glucocorticosteroids enhance intestinal uptake in mature animals. Maternal stimuli may cause intestinal adaptation in the offspring. We hypothesized that administering GLP-2, dexamethasone (DEX) or a combination of GLP-2+DEX to rat dams during pregnancy and lactation would enhance intestinal sugar uptake in their offspring. Rat dams were treated with GLP-2 (0.1 μg/g/day), DEX (0.128 μg/g/day), a combination of GLP-2+DEX or placebo. Glucose and fructose uptake was assessed in their suckling offspring using an in vitro intestinal ring uptake technique. The protein abundance of SGLT1, GLUT5, GLUT2, Na +K +-ATPase and selected signals was determined by immunohistochemistry; GLP-2 caused hypertrophy of the jejunal enterocytes and increased ileal villous height. Jejunal fructose uptake was reduced by GLP-2, DEX and GLP-2+DEX. V max for jejunal glucose uptake was reduced with DEX and GLP-2+DEX. These declines were not explained by alterations in transporter abundance. Decreases in Akt and mTOR abundance were associated with declines in transporter activity. We speculate that the intrinsic activity of the sugar transporters was modified via the P13K pathway. In conclusion, maternal GLP-2 and DEX reduced intestinal sugar uptake in their offspring. This may have nutritional implications for the offspring of mothers treated with GLP-2 or steroids.

Involvement of an enterocyte renin–angiotensin system in the local control of SGLT1‐dependent glucose uptake across the rat small intestinal brush border membrane

There is increasing evidence that locally produced angiotensin AII (AII) regulates the function of many tissues, but the involvement of enterocyte-derived AII in the control of intestinal transport is unknown. This study examined whether there is a local renin-angiotensin system (RAS) in rat villus enterocytes and assessed the effects of AII on SGLT1-dependent glucose transport across the brush border membrane (BBM). Gene and protein expression of angiotensinogen, ACE, and AT(1) and AT(2) receptors were studied in jejunal and ileal enterocytes using immunocytochemistry, Western blotting and RT-PCR. Mucosal uptake of d-[(14)C]glucose by everted intestinal sleeves before and after addition of AII (0-100 nm) to the mucosal buffer was measured in the presence or absence of the AT(1) receptor antagonist losartan (1 microm). Immunocytochemistry revealed the expression of angiotensinogen, ACE, and AT(1) and AT(2) receptors in enterocytes; immunoreactivity of AT(1) receptor and angiotensinogen proteins was especially pronounced at the BBM. Expression of angiotensinogen and AT(1) and AT(2) receptors, but not ACE, was greater in the ileum than the jejunum. Addition of AII to mucosal buffer inhibited phlorizin-sensitive (SGLT1-dependent) jejunal glucose uptake in a rapid and dose-dependent manner and reduced the expression of SGLT1 at the BBM. Losartan attenuated the inhibitory action of AII on glucose uptake. AII did not affect jejunal uptake of l-leucine. The detection of RAS components at the enterocyte BBM, and the rapid inhibition of SGLT1-dependent glucose uptake by luminal AII suggest that AII secretion exerts autocrine control of intestinal glucose transport.

Effect of In ovo Peptide YY on the Ontogeny of Glucose Transport in Turkey Poults

Previous studies in this laboratory have demonstrated that peptide YY (PYY) administration to turkey poults at d25 of incubation enhances intestinal Na-dependent active glucose uptake. This study was designed to further characterize the ontogeny of glucose transport in embryonic and hatchling poults and to investigate the effects of PYY on this process during development. In Trial 1, 20 turkey eggs were randomly selected at days 20, 23, and 26 of incubation, as well as the day of hatch. Hatchlings were cervically dislocated and the body weight, jejunal length and jejunal weight were recorded. Jejunal glucose uptake was estimated by measuring H-3-O-methyl-D-glucose accumulation in 2 mm jejunal rings in vitro. Jejunal O 3 2 consumption was measured in vitro on jejunal rings using an O probe. In Trial 2, 40 turkey eggs were 2 randomly selected at days 20, 23 and 25 of incubation and injected, via the air sac, with either 0.9% saline or 0.9 % saline plus 400 μg PYY/kg egg weight. Embryos from each treatment were harvested on days 23, 26 and day of hatch. Measurements and analyses on jejunal tissue were conducted as in Trial 1. In Trial 2, embryonic weight and jejunal weight adjusted for body weight increased (p<0.05) with stage of incubation, while adjusted jejunal length decreased (p<0.01). Active and total glucose uptake and jejunal O2 consumption increased with age (p<0.05). The energetic efficiency of glucose uptake increased (p<0.05) between d26 and hatch. In Trial 2, PYY failed to significantly affect body or jejunal weight, glucose absorption, and O consumption at any stage of development. PYY did however, decrease the efficiency of glucose 2 uptake at d26 and at hatch (p<0.05). In contrast to earlier investigations using higher dosages of PYY, this study demonstrated that in ovo PYY administration at 400 μg/kg egg weight has little effect of jejunal function in turkeys.

A Combination of Dexamethasone and Glucagon‐like Peptide‐2 Increase Intestinal Morphology and Glucose Uptake in Suckling Rats

Glucagon-like peptide (GLP)-2 enhances nutrient uptake in adult animals. Glucocorticosteroids accelerate intestinal ontogeny and increase nutrient uptake in adult animals. We hypothesized that administering GLP-2 and dexamethasone (DEX) to suckling rats will enhance sugar uptake and that this effect persists into the postweaning period. Suckling rats were treated for 10 days with GLP-2 (0.1 microg/g/d, twice daily), DEX (0.128 microg/g/d, once daily), GLP-2 + Dex (same doses as above), or placebo. The rate of intestinal uptake of glucose and fructose in sucklings (19-21 days old) and weanlings (49 days old) was assessed using an in vitro ring technique. DEX reduced body weight in weanlings, whereas GLP-2 + DEX prevented this effect. In sucklings, GLP-2 + DEX increased ileal villous height and jejunal and ileal villous width and crypt depth. In sucklings, GLP-2 + DEX increased the maximal transport rate (Vmax) for jejunal glucose uptake, whereas DEX reduced the ileal Vmax. In weanlings, GLP-2 + DEX increased jejunal villous height, whereas ileal villous width and crypt depth were reduced. DEX increased the ileal Vmax and apparent affinity constant for glucose in weanlings. The combination of these hormones may be useful in stimulating glucose uptake in the developing intestine, and giving DEX to sucklings may enhance glucose uptake in later life.

High-methoxyl pectin has greater enhancing effect on glucose uptake in intestinal perfused rats

Objective Pectins have been known to decrease blood glucose levels. However, the mechanism of this effect is unclear. The direct action of various pectins (high- or low-methoxyl pectins) on the intestinal absorption of glucose was investigated in gut-perfused rats. Methods After equilibrium, jejunal and ileal segments were simultaneously perfused with an isotonic electrolyte solution (pH 7.4) containing glucose (10 mM/L) and high- or low-methoxyl pectins (10 g/L). Each test or control solution was perfused in a random sequence, with perfusion times of 30 min. Changes in glucose concentration of perfusate solution reservoir were determined over the experimental period. Results High- and low-methoxyl pectins in the perfusate significantly inhibited jejunal uptake of glucose compared with the control ( P < 0.05). High-methoxyl pectins had greater inhibitive effect on intestinal absorption of glucose than low-methoxyl pectins. The observed changes in glucose and water absorptions caused by high- or low-methoxyl pectins were reversible by switching to a pectin-free perfusate. In addition, net water absorption changed to secretion after addition of high- or low-methoxyl pectins. Conclusions These results suggest that the decrease in intestinal absorption of glucose observed after perfusion of high- or low-methoxyl pectins may be caused by viscosity-related increases in mucosal unstirred layer thickness.