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1
Play, B., Z. Haikal, I. Fromont, O. Ghiringhelli, D. Lairon, and D. Jourdheuil-Rahmani. "C28 - Absorption intestinale du cholesterol : regulation par le glucose apical." Gastroentérologie Clinique et Biologique 30, no. 1 (January 2006): 87. http://dx.doi.org/10.1016/s0399-8320(06)73110-4.
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Cottrell, J. J., B. Stoll, R. K. Buddington, J. E. Stephens, L. Cui, X. Chang, and D. G. Burrin. "Glucagon-like peptide-2 protects against TPN-induced intestinal hexose malabsorption in enterally refed piglets." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 2 (February 2006): G293—G300. http://dx.doi.org/10.1152/ajpgi.00275.2005.
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Premature infants receiving chronic total parenteral nutrition (TPN) due to feeding intolerance develop intestinal atrophy and reduced nutrient absorption. Although providing the intestinal trophic hormone glucagon-like peptide-2 (GLP-2) during chronic TPN improves intestinal growth and morphology, it is uncertain whether GLP-2 enhances absorptive function. We placed catheters in the carotid artery, jugular and portal veins, duodenum, and a portal vein flow probe in piglets before providing either enteral formula (ENT), TPN or a coinfusion of TPN plus GLP-2 for 6 days. On postoperative day 7, all piglets were fed enterally and digestive functions were evaluated in vivo using dual infusion of enteral (13C) and intravenous (2H) glucose, in vitro by measuring mucosal lactase activity and rates of apical glucose transport, and by assessing the abundances of sodium glucose transporter-1 (SGLT-1) and glucose transporter-2 (GLUT2). Both ENT and GLP-2 pigs had larger intestine weights, longer villi, and higher lactose digestive capacity and in vivo net glucose and galactose absorption compared with TPN alone. These endpoints were similar in ENT and GLP-2 pigs except for a lower intestinal weight and net glucose absorption in GLP-2 compared with ENT pigs. The enhanced hexose absorption in GLP-2 compared with TPN pigs corresponded with higher lactose digestive and apical glucose transport capacities, increased abundance of SGLT-1, but not GLUT-2, and lower intestinal metabolism of [13C]glucose to [13C]lactate. Our findings indicate that GLP-2 treatment during chronic TPN maintains intestinal structure and lactose digestive and hexose absorptive capacities, reduces intestinal hexose metabolism, and may facilitate the transition to enteral feeding in TPN-fed infants.
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Leonie Los, E., Henk Wolters, Frans Stellaard, Folkert Kuipers, Henkjan J. Verkade, and Edmond H. H. M. Rings. "Intestinal capacity to digest and absorb carbohydrates is maintained in a rat model of cholestasis." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 3 (September 2007): G615—G622. http://dx.doi.org/10.1152/ajpgi.00188.2007.
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Cholestasis is associated with systemic accumulation of bile salts and with deficiency of bile in the intestinal lumen. During the past years bile salts have been identified as signaling molecules that regulate lipid, glucose, and energy metabolism. Bile salts have also been shown to activate signaling routes leading to proliferation, apoptosis, or differentiation. It is unclear, however, whether cholestasis affects the constitution and absorptive capacity of the intestinal epithelium in vivo. We studied small intestinal morphology, proliferation, apoptosis, expression of intestine-specific genes, and carbohydrate absorption in cholestatic (1 wk bile duct ligation), bile-deficient (1 wk bile diversion), and control (sham) rats. Absorptive capacity was assessed by determination of plasma [2H]- and [13C]glucose concentrations after intraduodenal administration of [2H]glucose and naturally enriched [13C]sucrose, respectively. Small intestinal morphology, proliferation, apoptosis, and gene expression of intestinal transcription factors (mRNA levels of Cdx-2, Gata-4, and Hnf-1α, and Cdx-2 protein levels) were similar in cholestatic, bile-deficient, and control rats. The (unlabeled) blood glucose response after intraduodenal administration was delayed in cholestatic animals, but the absorption over 180 min was quantitatively similar between the groups. Plasma concentrations of [2H]glucose and [13C]glucose peaked to similar extents in all groups within 7.5 and 30 min, respectively. Absorption of [2H]glucose and [13C]glucose in plasma was similar in all groups. The present data indicate that neither accumulation of bile salts in the body, nor their intestinal deficiency, two characteristic features of cholestasis, affect rat small intestinal proliferation, differentiation, apoptosis, or its capacity to digest and absorb carbohydrates.
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Balakrishnan, A. "Micromanaging the gut: unravelling the regulatory pathways that mediate the intestinal adaptive response." Annals of The Royal College of Surgeons of England 100, no. 3 (March 2018): 165–71. http://dx.doi.org/10.1308/rcsann.2017.0174.
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Short bowel syndrome occurs following the loss of a large portion of functional intestine and is associated with high morbidity and mortality. The intestine exhibits pronounced diurnal rhythms in glucose absorption and mounts a profound proliferative response following massive small bowel resection. Understanding the molecular pathways that underpin this could yield novel treatment options. Two in vivo models were employed using the nocturnally active Sprague Dawley® rat, namely daytime feeding and massive small bowel resection. Glucose absorption exhibited a 24-hour periodicity in the gut and peaked during maximal nutrient delivery, mediated by rhythms in the glucose transporter sodium glucose co-transporter 1 (SGLT1). Feeding during the day shifted the peak in the circadian clock gene PER1 and SGLT1. RNA interference and luciferase assays demonstrated that PER1 transcriptionally regulates SGLT1, linking for the first time clock genes and intestinal glucose absorption. Intestinal proliferation also exhibited diurnal rhythmicity, with peak absorptive surface area occurring during maximal nutrient availability. mir-16 is diurnally expressed in intestinal crypts, exhibiting minimal expression during maximal nutritional availability. mir-16 overexpression increased apoptosis and arrested proliferation in vitro. mir-125a was upregulated in intestinal crypts following 80% small bowel resection, and induced apoptosis and growth arrest upon overexpression in vitro. This work provides novel insights into the role of circadian clock genes, intestinal transporters and microRNAs in regulating intestinal absorption and proliferation and is the first demonstration of a role for microRNAs in these adaptive phenomena. Modulation of these pathways may represent a new therapeutic option for the management of short bowel syndrome.
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Stümpel, Frank, Tomas Kucera, and Kurt Jungermann. "Impaired stimulation of intestinal glucose absorption via hepatoenteral nerves in streptozotocin-diabetic rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 2 (August 1, 1999): G285—G291. http://dx.doi.org/10.1152/ajpgi.1999.277.2.g285.
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In an ex situ organ perfusion system, that of the isolated nonrecirculating joint perfusion of rat small intestine and liver, insulin infused into the portal vein increased intestinal glucose absorption. This insulin action against the bloodstream can be blocked by TTX, indicating a propagation of the insulin signal via hepatoenteral nerves, which conforms with previous studies with atropine and carbachol. Insulin action could also be mimicked by dibutyryl cAMP (DBcAMP) acting directly on the absorptive enterocytes. Because autonomic neuropathy is a common late complication of diabetes mellitus, the possible impairment of these nerves in the diabetic state was studied in streptozotocin-diabetic rats. In the isolated joint intestine-liver perfusion, glucose was applied as a bolus into the lumen; its absorption was measured in the portal vein. In 5-day diabetic as well as in control rats, portal insulin, arterial carbachol, and arterial DBcAMP increased intestinal glucose absorption. In 3-mo diabetic rats portal insulin and arterial carbachol failed to stimulate glucose absorption, whereas arterial DBcAMP still did so, indicating an undisturbed function of the absorptive enterocytes. The lack of an effect of portal insulin and arterial carbachol and the unchanged action of DBcAMP in the chronically diabetic rats indicated that the signaling chain via the hepatoenteral nerves was impaired, which is in line with a diabetic neuropathy.
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Dyer, J., K. Daly, K. S. H. Salmon, D. K. Arora, Z. Kokrashvili, R. F. Margolskee, and S. P. Shirazi-Beechey. "Intestinal glucose sensing and regulation of intestinal glucose absorption." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 1191–94. http://dx.doi.org/10.1042/bst0351191.
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SGLT1 (Na+/glucose co-transporter 1) transports the dietary sugars, D-glucose and D-galactose, from the lumen of the intestine into enterocytes. SGLT1 regulation has important consequences for the provision of glucose to the respiring tissues and is therefore essential for maintaining glucose homoeostasis. SGLT1 expression is directly regulated in response to changes in the sugar content of the diet. To monitor these variations, there is a requirement for a glucose-sensing system located on the luminal membrane of gut cells. This short review focuses on recent findings on intestinal sugar sensing and the downstream mechanisms responsible for enhancement in SGLT1 expression.
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Gromova, Lyudmila V., Serguei O. Fetissov, and Andrey A. Gruzdkov. "Mechanisms of Glucose Absorption in the Small Intestine in Health and Metabolic Diseases and Their Role in Appetite Regulation." Nutrients 13, no. 7 (July 20, 2021): 2474. http://dx.doi.org/10.3390/nu13072474.
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The worldwide prevalence of metabolic diseases such as obesity, metabolic syndrome and type 2 diabetes shows an upward trend in recent decades. A characteristic feature of these diseases is hyperglycemia which can be associated with hyperphagia. Absorption of glucose in the small intestine physiologically contributes to the regulation of blood glucose levels, and hence, appears as a putative target for treatment of hyperglycemia. In fact, recent progress in understanding the molecular and cellular mechanisms of glucose absorption in the gut and its reabsorption in the kidney helped to develop a new strategy of diabetes treatment. Changes in blood glucose levels are also involved in regulation of appetite, suggesting that glucose absorption may be relevant to hyperphagia in metabolic diseases. In this review we discuss the mechanisms of glucose absorption in the small intestine in physiological conditions and their alterations in metabolic diseases as well as their relevance to the regulation of appetite. The key role of SGLT1 transporter in intestinal glucose absorption in both physiological conditions and in diabetes was clearly established. We conclude that although inhibition of small intestinal glucose absorption represents a valuable target for the treatment of hyperglycemia, it is not always suitable for the treatment of hyperphagia. In fact, independent regulation of glucose absorption and appetite requires a more complex approach for the treatment of metabolic diseases.
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Wang, Yun, Zhangjian Chen, Shi Chen, Lin Zhuo, Lin Zhao, and Guang Jia. "Effect of Short-Term Exposure to Titanium Dioxide Nanoparticles on Intestinal Absorption of Glucose by Ex Vivo Everted Rat Gut Sac Model." Journal of Nanoscience and Nanotechnology 21, no. 9 (September 1, 2021): 4586–95. http://dx.doi.org/10.1166/jnn.2021.19350.
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Titanium dioxide nanoparticles (TiO2 NPs) as food additives were widely found in various foodrelated products, especially in high-sugar foods. The daily intake of TiO2 NPs in the diet may therefore expose the small intestine to TiO2 NPs and affect its physiological functions, including the absorption of nutrients. It is speculated that TiO2 may cause serious health hazards by increasing sugar uptake. To explore this possibility, transport of glucose from small intestine was studied using an everted gut sac model prepared from small intestine of young healthy male SD rats. The translocation of TiO2 NPs and the morphological changes of small intestine were also observed after exposure of intestinal lumen to TiO2 NPs for 2 h. The results showed that TiO2 NPs can enter into enterocyte but hardly cross the intestinal epithelium. No change on microstructure of gut epithelia and expression of glucose transporter was found, and there is no obvious impact on intestinal absorption and metabolism of glucose. These results suggest that short-term exposure to TiO2 NPs has little influence on intestinal absorption of glucose. More attention should be paid to the chronic effect of dietary consumption of TiO2 NPs on nutrient absorption.
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Rhoads, J. M., E. O. Keku, L. E. Bennett, J. Quinn, and J. G. Lecce. "Development of L-glutamine-stimulated electroneutral sodium absorption in piglet jejunum." American Journal of Physiology-Gastrointestinal and Liver Physiology 259, no. 1 (July 1, 1990): G99—G107. http://dx.doi.org/10.1152/ajpgi.1990.259.1.g99.
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Glutamine is the primary metabolic fuel of the small intestine. To determine the effects of glutamine on intestinal electrolyte transport, piglet (3 days to 3 wk old) jejunum was bathed in Ussing chambers in a buffer containing 10 mM serosal glucose, and the effects of different concentrations of mucosal L-glutamine and D-glucose on short-circuit current and transmucosal Na+ and Cl- transport were measured. Resting jejunum secreted Na+ and Cl- in an electrogenic manner. In contrast to mucosal D-glucose (30 mM), which promoted electrogenic Na+ absorption (1.8 mueq.cm-2.h-1), mucosal L-glutamine (30 mM) stimulated both Na+ (2.7 mueq.cm-2.h-1) and Cl- (2.2 mueq.cm-2.h-1) absorption. This NaCl-absorptive jejunal response depended on the presence of both Na+ and Cl-, did not appear until animals were greater than 7 days of age, and was not observed with glucose, phenylalanine, or mannitol. Serosal, as well as mucosal, glutamine (30 mM) promoted electroneutral NaCl absorption. A small electrogenic Na(+)-absorptive response to L-glutamine was also observed. The effect of L-glutamine on jejunal NaCl transport resembles that of other metabolic fuels on colonic transport; its mechanism remains to be determined. We conclude that glutamine promotes electroneutral salt absorption in the small intestine.
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Inoue, Makoto, Yuichi Tanaka, Sakiko Matsushita, Yuri Shimozaki, Hirohito Ayame, and Hidenori Akutsu. "Xenogeneic-Free Human Intestinal Organoids for Assessing Intestinal Nutrient Absorption." Nutrients 14, no. 3 (January 19, 2022): 438. http://dx.doi.org/10.3390/nu14030438.
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Since many nutrients, including the three major ones of glucose, dipeptides, and cholesterol, are mainly absorbed in the small intestine, the assessment of their effects on intestinal tissue is important for the study of food absorption. However, cultured intestinal cell lines, such as Caco-2 cells, or animal models, which differ from normal human physiological conditions, are generally used for the evaluation of intestinal absorption and digestion. Therefore, it is necessary to develop an alternative in vitro method for more accurate analyses. In this study, we demonstrate inhibitory effects on nutrient absorption through nutrient transporters using three-dimensional xenogeneic-free human intestinal organoids (XF-HIOs), with characteristics of the human intestine, as we previously reported. We first show that the organoids absorbed glucose, dipeptide, and cholesterol in a transporter-dependent manner. Next, we examine the inhibitory effect of natural ingredients on the absorption of glucose and cholesterol. We reveal that glucose absorption was suppressed by epicatechin gallate or nobiletin, normally found in green tea catechin or citrus fruits, respectively. In comparison, cholesterol absorption was not inhibited by luteolin and quercetin, contained in some vegetables. Our findings highlight the usefulness of screening for the absorption of functional food substances using XF-HIOs.
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Yang, Jiufang, Theo H. van Dijk, Martijn Koehorst, Rick Havinga, Jan Freark de Boer, Folkert Kuipers, and Tim van Zutphen. "Intestinal Farnesoid X Receptor Modulates Duodenal Surface Area but Does Not Control Glucose Absorption in Mice." International Journal of Molecular Sciences 24, no. 4 (February 18, 2023): 4132. http://dx.doi.org/10.3390/ijms24044132.
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Bile acids facilitate the intestinal absorption of dietary lipids and act as signalling molecules in the maintenance of metabolic homeostasis. Farnesoid X receptor (FXR) is a bile acid-responsive nuclear receptor involved in bile acid metabolism, as well as lipid and glucose homeostasis. Several studies have suggested a role of FXR in the control of genes regulating intestinal glucose handling. We applied a novel dual-label glucose kinetic approach in intestine-specific FXR−/− mice (iFXR-KO) to directly assess the role of intestinal FXR in glucose absorption. Although iFXR-KO mice showed decreased duodenal expression of hexokinase 1 (Hk1) under obesogenic conditions, the assessment of glucose fluxes in these mice did not show a role for intestinal FXR in glucose absorption. FXR activation with the specific agonist GS3972 induced Hk1, yet the glucose absorption rate remained unaffected. FXR activation increased the duodenal villus length in mice treated with GS3972, while stem cell proliferation remained unaffected. Accordingly, iFXR-KO mice on either chow, short or long-term HFD feeding displayed a shorter villus length in the duodenum compared to wild-type mice. These findings indicate that delayed glucose absorption reported in whole-body FXR−/− mice is not due to the absence of intestinal FXR. Yet, intestinal FXR does have a role in the small intestinal surface area.
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Philpott, D. J., J. D. Butzner, and J. B. Meddings. "Regulation of intestinal glucose transport." Canadian Journal of Physiology and Pharmacology 70, no. 9 (September 1, 1992): 1201–7. http://dx.doi.org/10.1139/y92-167.
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The small intestine is capable of adapting nutrient transport in response to numerous stimuli. This review examines several possible mechanisms involved in intestinal adaptation. In some cases, the enhancement of transport is nonspecific, that is, the absorption of many nutrients is affected. Usually, increased transport capacity in these instances can be attributed to an increase in intestinal surface area. Alternatively, some conditions induce specific regulation at the level of the enterocyte that affects the transport of a particular nutrient. Since the absorption of glucose from the intestine is so well characterized, it serves as a useful model for this type of intestinal adaptation. Four potential sites for the specific regulation of glucose transport have been described, and each is implicated in different situations. First, mechanisms at the brush-border membrane of the enterocyte are believed to be involved in the upregulation of glucose transport that occurs in streptozotocin-induced diabetes mellitus and alterations in dietary carbohydrate levels. Also, factors that increase the sodium gradient across the enterocyte may increase the rate of glucose transport. It has been suggested that an increase in activity of the basolaterally located Na+–K+ ATPase could be responsible for this phenomena. The rapid increase in glucose uptake seen in hyperglycemia seems to be mediated by an increase in both the number and activity of glucose carriers located at the basolateral membrane. More recently, it was demonstrated that mechanisms at the basolateral membrane also play a role in the chronic increase in glucose transport observed when dietary carbohydrate levels are increased. Finally, alterations in tight-junction permeability enhance glucose absorption from the small intestine. The possible signals that prompt these adaptive responses in the small intestine include glucose itself and humoral as well as enteric nervous interactions.Key words: intestinal transport, glucose transport, intestinal adaptation.
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Wang, L. F., H. Luo, M. Miyoshi, T. Imoto, Y. Hiji, and T. Sasaki. "Inhibitory effect of gymnemic acid on intestinal absorption of oleic acid in rats." Canadian Journal of Physiology and Pharmacology 76, no. 10-11 (October 1, 1998): 1017–23. http://dx.doi.org/10.1139/y98-123.
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Gymnemic acid, a mixture of triterpene glycosides extracted from the leaves of Gymnema sylvestre, is known to inhibit the intestinal absorption of glucose in human and rats. This work examined the effect of gymnemic acid on oleic acid absorption by the method of intestinal perfusion in rats. The results showed the following. (i) Gymnemic acid potently inhibited the absorption of oleic acid in intestine. (ii) This inhibition was dose dependent and reversible. (iii) The extent of inhibition and the recovery progress were extremely similar to that of glucose absorption. (iv) Taurocholate did not affect the inhibitory effect of gymnemic acid on oleic acid absorption, but lowering its concentration facilitated the recovery from the inhibition. (v) The absorption of oleic acid was not affected by other glycosides such as phloridzin, stevioside, and glycyrrhizin. These new findings are important for understanding the roles of gymnemic acid in therapy of diabetes mellitus and obesity.Key words: gymnemic acid, oleic acid, glucose, intestinal absorption, rat.
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White, J. F., K. Burnup, and D. Ellingsen. "Effect of sugars and amino acids on amphibian intestinal Cl- transport and intracellular Na+, K+, and Cl- activity." American Journal of Physiology-Gastrointestinal and Liver Physiology 250, no. 1 (January 1, 1986): G109—G117. http://dx.doi.org/10.1152/ajpgi.1986.250.1.g109.
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The effect of glucose, galactose, and valine on intestinal Cl- transport and intracellular Cl-, Na+, and K+ activity was investigated in isolated segments of Amphiuma small intestine. By use of double-barreled Cl- -specific microelectrodes, it was observed that galactose and valine reduced the luminal membrane potential (psi m) and eliminated the difference between the Cl- equilibrium potential (ECl) and psi m, i.e., the Cl- accumulation potential (ECl-psi m) approached zero. Simultaneously, Cl- absorption (JnetCl) was reduced in short-circuited tissues and Na+ absorption was enhanced. In contrast, after exposure to glucose, psi m and ECl-psi m declined only transiently and JnetCl was unaltered. In tissues pretreated with galactose to reduce Cl- transport, addition of glucose to the serosal medium restored Cl- accumulation across the luminal membrane and the Cl- absorptive current. Glucose, galactose, and valine each reduced intracellular K+ activity significantly. Galactose and valine each increased [corrected] intracellular Na activity (aiNa) markedly, whereas glucose increased aiNa only slightly. In conclusion, intestinal ion transport can be limited by the availability of metabolic substrate. The nonmetabolized solutes galactose and valine inhibited Cl- uptake and net Cl- absorption while stimulating net Na absorption, as though net Na+ absorption has priority over Cl- transport at the cellular level. Cl- transport is reduced at both mucosal and serosal membranes. At the luminal membrane electrogenic Cl- uptake is slowed or a backleak of Cl- is enhanced; at the serosal membrane Cl- exchange with Na+ (and HCO3-) driven by the Na+ gradient is reduced. The availability of metabolizable glucose to the cell prevents the reduction in net Cl- absorption.
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Yamamoto, Kana, Norio Harada, Takuma Yasuda, Tomonobu Hatoko, Naoki Wada, Xuejing Lu, Youhei Seno, Takashi Kurihara, Shunsuke Yamane, and Nobuya Inagaki. "Intestinal Morphology and Glucose Transporter Gene Expression under a Chronic Intake of High Sucrose." Nutrients 16, no. 2 (January 7, 2024): 196. http://dx.doi.org/10.3390/nu16020196.
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Sucrose is a disaccharide that is degraded into fructose and glucose in the small intestine. High-sucrose and high-fructose diets have been reported, using two-dimensional imaging, to alter the intestinal morphology and the expression of genes associated with sugar transport, such as sodium glucose co-transporter 1 (SGLT1), glucose transporter 2 (GLUT2), and glucose transporter 5 (GLUT5). However, it remains unclear how high-fructose and high-sucrose diets affect the expression of sugar transporters and the intestinal morphology in the whole intestine. We investigate the influence of a chronic high-sucrose diet on the expression of the genes associated with sugar transport as well as its effects on the intestinal morphology using 3D imaging. High sucrose was found to increase GLUT2 and GLUT5 mRNA levels without significant changes in the intestinal morphology using 3D imaging. On the other hand, the delay in sucrose absorption by an α-glucosidase inhibitor significantly improved the intestinal morphology and the expression levels of SGLT1, GLUT2, and GLUT5 mRNA in the distal small intestine to levels similar to those in the proximal small intestine, thereby improving glycemic control after both glucose and sucrose loading. These results reveal the effects of chronic high-sugar exposure on glucose absorption and changes in the intestinal morphology.
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Zheng, Lin, Pengfei Hou, Jinjin Jing, Min Zhou, Le Wang, Luting Wu, Jundong Zhu, Long Yi, and Mantian Mi. "Pterostilbene Attenuates High-Intensity Swimming Exercise-Induced Glucose Absorption Dysfunction Associated with the Inhibition of NLRP3 Inflammasome-Induced IECs Pyroptosis." Nutrients 15, no. 9 (April 23, 2023): 2036. http://dx.doi.org/10.3390/nu15092036.
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The study investigated the effect of pterostilbene (PTE) on intestinal glucose absorption and its underlying mechanisms in high-intensity swimming exercise (HISE)-treated mice. Male C57BL/6 mice were treated with PTE for 4 weeks and performed high-intensity swimming training in the last week. Intestinal epithelial cells (IECs) were pretreated with 0.5 and 1.0 μM PTE for 24 h before being incubated in hypoxia/reoxygenation condition. Intestinal glucose absorption was detected by using an oral glucose tolerance test and d-xylose absorption assay, and the levels of factors related to mitochondrial function and pyroptosis were measured via western blot analyses, cell mito stress test, and quantitative real-time polymerase chain reaction. In vivo and in vitro, the results showed that PTE attenuated HISE-induced intestinal glucose absorption dysfunction and pyroptosis in mice intestine. Moreover, PTE inhibited NLRP3 inflammasome and the mitochondrial homeostasis as well as the ROS accumulation in IEC in vitro. Additionally, knockdown of SIRT3, a major regulator of mitochondria function, by siRNA or inhibiting its activity by 3-TYP abolished the effects of PTE on pyroptosis, mitochondrial homeostasis, and ROS generation of IEC in vitro. Our results revealed that PTE could alleviate HISE-induced intestinal glucose absorption dysfunction associated with the inhibition of NLRP3 inflammasome-induced IECs pyroptosis.
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Lane, John S., Edward E. Whang, David A. Rigberg, Oscar J. Hines, David Kwan, Michael J. Zinner, David W. McFadden, Jared Diamond, and Stanley W. Ashley. "Paracellular glucose transport plays a minor role in the unanesthetized dog." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 3 (March 1, 1999): G789—G794. http://dx.doi.org/10.1152/ajpgi.1999.276.3.g789.
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Traditionally, intestinal glucose absorption was thought to occur through active, carrier-mediated transport. However, proponents of paracellular transport have argued that previous experiments neglected effects of solvent drag coming from high local concentrations of glucose at the brush-border membrane. The purpose of this study was to evaluate glucose absorption in the awake dog under conditions that would maximize any contribution of paracellular transport. Jejunal Thiry-Vella loops were constructed in six female mongrel dogs. After surgical recovery, isotonic buffers containingl-glucose as the probe for paracellular permeability were given over 2-h periods by constant infusion pump. At physiological concentrations ofd-glucose (1–50 mM), the fractional absorption ofl-glucose was only 4–7% of total glucose absorption. Infusion of supraphysiological concentrations (150 mM) of d-glucose,d-maltose, ord-mannitol yielded low-fractional absorptions ofl-glucose (2–5%), so too did complex or nonabsorbable carbohydrates. In all experiments, there was significant fractional water absorption (5–19%), a prerequisite for solvent drag. Therefore, with even up to high concentrations of luminal carbohydrates in the presence of significant water absorption, the relative contribution of paracellular glucose absorption remained low.
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Rhoads, J. M., E. O. Keku, J. P. Woodard, S. I. Bangdiwala, J. G. Lecce, and J. T. Gatzy. "L-glutamine with D-glucose stimulates oxidative metabolism and NaCl absorption in piglet jejunum." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 6 (December 1, 1992): G960—G966. http://dx.doi.org/10.1152/ajpgi.1992.263.6.g960.
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To explore the relationship between intestinal fluid absorption and oxidative metabolism, we measured the effects of amino acids and glucose on piglet jejunal ion transport and oxygen consumption (QO2) in vitro. Jejunal QO2 was stimulated by L-glutamine and D-glucose but not by the nonmetabolizable organic solutes methyl beta-D-glucoside or L-phenylalanine. QO2 was maximally enhanced by the combination of D-glucose and L-glutamine (5 mM). Even though 5 mM L-glutamine was previously found to be insufficient to stimulate NaCl absorption, 5 mM L-glutamine enhanced jejunal NaCl flux when combined with equimolar mucosal D-glucose. Either D-glucose or methyl beta-D-glucoside caused an increase in short-circuit current (Isc), an increase in Na+ absorption in excess of Isc, and a decrease in Cl- secretion, when L-glutamine was substituted for D-glucose (10 mM) on the serosal side. This relationship suggests that mucosal sugars, if combined with L-glutamine, enhance neutral NaCl absorption as well as electrogenic Na+ flow. (Aminooxy)acetate, an inhibitor of alanine aminotransferase, abolished the stimulation of QO2 and the NaCl-absorptive response to L-glutamine. We conclude that the oxidative metabolism fueled by L-glutamine is linked to a NaCl-absorptive mechanism in the intestine. We propose that the CO2 produced by glutamine metabolism yields carbonic acid, which dissociates to H+ and HCO3-, which may stimulate parallel antiports in the apical membrane.
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Wu, Tongzhi, Christopher K. Rayner, Karen L. Jones, Cong Xie, Chinmay Marathe, and Michael Horowitz. "Role of intestinal glucose absorption in glucose tolerance." Current Opinion in Pharmacology 55 (December 2020): 116–24. http://dx.doi.org/10.1016/j.coph.2020.10.017.
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Rhodes, Ryon Sun S., Satish K. Singh, Vazhaikkurichi M. Rajendran, Seth T. Walk, and Steven D. Coon. "Regulation of Glucose Insulinotropic Peptide and Intestinal Glucose Transporters in the Diet-Induced Obese Mouse." Journal of Diabetes Research 2022 (February 17, 2022): 1–8. http://dx.doi.org/10.1155/2022/5636499.
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Our recent studies have shown that glucose-dependent insulinotropic polypeptide (GIP), but not glucagon-like peptide 1 (GLP-1), augments Na-glucose transporter 1- (SGLT1-) mediated glucose absorption in mouse jejunum. Na-dependent glucose absorption sharply rose and peaked in 3 months of high-fat (i.e., obese) compared to normal (i.e., normal weight) diet fed animals. Previous studies have shown that GIP-augmented SGLT1 and PEPT1 (peptide transporter 1) are regulated by protein kinase A (PKA) signaling in mouse jejunum. Additional studies have indicated that cAMP and PI3 kinase signaling augment PEPT1 through EPAC and AKT activation pathways, respectively, through increased apical PEPT1 trafficking in intestinal epithelial cells. However, little is known about how the signaling glucose transport paradigm is altered over a long period. Early on, increased glucose absorption occurs through SGLT1, but as the obesity and diabetes progress, there is a dramatic shift towards a Na-independent mechanism. Surprisingly, at the peak of glucose absorption during the fifth month of the progression of obesity, the SGLT1 activity was severely depressed, while a Na-independent glucose absorptive process begins to appear. Since glucose transporter 2 (GLUT2) is expressed on the apical membrane of the small intestine in obese patients and animal models of obesity, it was hypothesized to be the new more efficient route. Western blot analyses and biotinylation of the apical membrane revealed that the GIP expression increases in the obese animals and its trafficking to the apical membrane increases with the GIP treatment.
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Napier, Kathryn R., Cromwell Purchase, Todd J. McWhorter, Susan W. Nicolson, and Patricia A. Fleming. "The sweet life: diet sugar concentration influences paracellular glucose absorption." Biology Letters 4, no. 5 (June 17, 2008): 530–33. http://dx.doi.org/10.1098/rsbl.2008.0253.
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Small birds and bats face strong selection pressure to digest food rapidly in order to reduce digesta mass carried during flight. One mechanism is rapid absorption of a high proportion of glucose via the paracellular pathway (transfer between epithelial cells, not mediated by transporter proteins). Intestinal paracellular permeability to glucose was assessed for two nectarivorous passerines, the Australian New Holland honeyeater ( Phylidonyris novaehollandiae ) and African white-bellied sunbird ( Cinnyris talatala ) by measuring the bioavailability of radiolabelled, passively absorbed l -glucose. Bioavailability was high in both species and increased with diet sugar concentration (honeyeaters, 37 and 81% and sunbirds, 53 and 71% for 250 and 1000 mmol l −1 sucrose diets, respectively). We conclude that the relative contribution of paracellular to total glucose absorption increases with greater digesta retention time in the intestine, and paracellular absorption may also be modulated by factors such as intestinal lumen osmolality and interaction with mediated glucose uptake. The dynamic state of paracellular absorption should be taken into account in future studies.
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Lee, H. H., A. S. Prasad, G. J. Brewer, and C. Owyang. "Zinc absorption in human small intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 1 (January 1, 1989): G87—G91. http://dx.doi.org/10.1152/ajpgi.1989.256.1.g87.
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We determined the intestinal site of zinc absorption in humans and investigated the interaction between intestinal absorption of zinc and other solutes using the triple-lumen steady-state perfusion technique. Twenty-one healthy subjects participated in the study. During intestinal perfusion of a balanced electrolyte solution containing 0.1 mM zinc acetate, zinc absorption occurred throughout the entire small intestine. However, the jejunum had the highest rate of absorption (357 +/- 14 nM.min-1.40 cm-1) compared with the duodenum (230 +/- 33 nM.min-1.40 cm-1) and ileum (84 +/- 10 nM.min-1.40 cm-1). Over a range of zinc concentrations infused into the jejunum (0.1, 0.9, and 1.8 mM) there were linear increases in the rate of zinc absorption (P less than 0.05). Intestinal absorption of zinc was significantly stimulated by the addition of glucose (20 mM). Zinc absorption increased from 459 +/- 39 to 582 +/- 45 nM.min-1.40 cm-1 (P less than 0.05). Conversely, zinc (0.9 mM) also enhanced the absorption of glucose, which was increased from 293 +/- 43 to 447 +/- 27 microM.min-1.40 cm-1 (P less than 0.05). The enhanced absorption of zinc or glucose was not accompanied by any increase in absorption of water and sodium. In contrast, increasing the concentration of zinc in the perfusate resulted in decreased absorption of sodium and water in a dose-related manner. In conclusion, our study demonstrated that zinc absorption is concentration dependent and occurs throughout the small intestine. The jejunum has the highest rate of absorption of zinc. The interactions between absorption of zinc and other solutes suggest that the transport process of zinc is carrier mediated.
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Chan, Leo Ka Yu, and Po Sing Leung. "Multifaceted interplay among mediators and regulators of intestinal glucose absorption: potential impacts on diabetes research and treatment." American Journal of Physiology-Endocrinology and Metabolism 309, no. 11 (December 1, 2015): E887—E899. http://dx.doi.org/10.1152/ajpendo.00373.2015.
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Glucose is the prominent molecule that characterizes diabetes and, like the vast majority of nutrients in our diet, it is absorbed and enters the bloodstream directly through the small intestine; hence, small intestine physiology impacts blood glucose levels directly. Accordingly, intestinal regulatory modulators represent a promising avenue through which diabetic blood glucose levels might be moderated clinically. Despite the critical role of small intestine in blood glucose homeostasis, most physiological diabetes research has focused on other organs, such as the pancreas, kidney, and liver. We contend that an improved understanding of intestinal regulatory mediators may be fundamental for the development of first-line preventive and therapeutic interventions in patients with diabetes and diabetes-related diseases. This review summarizes the major important intestinal regulatory mediators, discusses how they influence intestinal glucose absorption, and suggests possible candidates for future diabetes research and the development of antidiabetic therapeutic agents.
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Li, Ping, Yan Hao, Feng-Hui Pan, Min Zhang, Jian-Qiang Ma, and Da-Long Zhu. "SGK1 inhibitor reverses hyperglycemia partly through decreasing glucose absorption." Journal of Molecular Endocrinology 56, no. 4 (May 2016): 301–9. http://dx.doi.org/10.1530/jme-15-0285.
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This study investigates the effectiveness and mechanisms of a serum- and glucocorticoid-inducible kinase 1 (SGK1) inhibitor in counteracting hyperglycemia. In an in vivo experiment, we demonstrated that after an 8-week treatment with an SGK1 inhibitor, the fasting blood glucose and HbA1c level significantly decreased in db/db mice. RT-PCR and western blot analyses revealed that intestinal SGK1 and sodium glucose co-transporter 1 (SGLT1) expression were enhanced in db/db mice. Treatment with an SGK1 inhibitor decreased excessive SGLT1 expression in the intestine of db/db mice. In vitro experiments with intestinal IEC-6 cells showed that the co-administration of an SGK1 inhibitor partly reversed the SGLT1 expression and glucose absorption that were induced by dexamethasone. In conclusion, this study revealed that the favorable effect of an SGK1 inhibitor on hyperglycemia is partly due to decreased glucose absorption through SGLT1 in the small intestine. These data collectively suggest that SGK1 may be a potent target for the treatment of diabetes and other metabolic disorders.
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Naftalin, Richard J. "A computer model simulating human glucose absorption and metabolism in health and metabolic disease states." F1000Research 5 (April 12, 2016): 647. http://dx.doi.org/10.12688/f1000research.8299.1.
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A computer model designed to simulate integrated glucose-dependent changes in splanchnic blood flow with small intestinal glucose absorption, hormonal and incretin circulation and hepatic and systemic metabolism in health and metabolic diseases e.g. non-alcoholic fatty liver disease, (NAFLD), non-alcoholic steatohepatitis, (NASH) and type 2 diabetes mellitus, (T2DM) demonstrates how when glucagon-like peptide-1, (GLP-1) is synchronously released into the splanchnic blood during intestinal glucose absorption, it stimulates superior mesenteric arterial (SMA) blood flow and by increasing passive intestinal glucose absorption, harmonizes absorption with its distribution and metabolism. GLP-1 also synergises insulin-dependent net hepatic glucose uptake (NHGU). When GLP-1 secretion is deficient post-prandial SMA blood flow is not increased and as NHGU is also reduced, hyperglycaemia follows. Portal venous glucose concentration is also raised, thereby retarding the passive component of intestinal glucose absorption. Increased pre-hepatic sinusoidal resistance combined with portal hypertension leading to opening of intrahepatic portosystemic collateral vessels are NASH-related mechanical defects that alter the balance between splanchnic and systemic distributions of glucose, hormones and incretins.The model reveals the latent contribution of portosystemic shunting in development of metabolic disease. This diverts splanchnic blood content away from the hepatic sinuses to the systemic circulation, particularly during the glucose absorptive phase of digestion, resulting in inappropriate increases in insulin-dependent systemic glucose metabolism. This hastens onset of hypoglycaemia and thence hyperglucagonaemia. The model reveals that low rates of GLP-1 secretion, frequently associated with T2DM and NASH, may be also be caused by splanchnic hypoglycaemia, rather than to intrinsic loss of incretin secretory capacity. These findings may have therapeutic implications on GLP-1 agonist or glucagon antagonist usage.
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Sangild, Per T., Christiane Malo, Mette Schmidt, Yvette M. Petersen, Jan Elnif, Jens J. Holst, and Randal K. Buddington. "Glucagon-like peptide 2 has limited efficacy to increase nutrient absorption in fetal and preterm pigs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 6 (December 2007): R2179—R2184. http://dx.doi.org/10.1152/ajpregu.00395.2007.
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Exogenous glucagon-like peptide 2 (GLP-2) prevents intestinal atrophy and increases nutrient absorption in term newborn pigs receiving total parenteral nutrition (TPN). We tested the hypothesis that the immature intestine of fetuses and preterm neonates has a diminished nutrient absorption response to exogenous GLP-2. This was accomplished using catheterized fetal pigs infused for 6 days (87–91% of gestation) with GLP-2 (25 nmol·kg−1·day−1 iv; n = 7) or saline ( n = 7), and cesarean-delivered preterm pigs (92% of gestation) that received TPN with GLP-2 (25 nmol·kg−1·day−1 iv; n = 8) or saline ( n = 7) for 6 days after birth. Responses to GLP-2 were assessed by measuring intestinal dimensions, absorption of nutrients (glucose, leucine, lysine, proline) by intact tissues and brush border membrane vesicles, and abundance of sodium-glucose cotransporter mRNA. Infusion of GLP-2 increased circulating GLP-2 levels in fetuses, but did not increase intestinal mass or absorption of nutrients by intact tissues and brush border membrane vesicles, except for lysine. Administration of exogenous GLP-2 to preterm TPN-fed pigs similarly did not increase rates of nutrient absorption, yet nutrient absorption capacities of the entire small intestine tended to increase (+10–20%, P < 0.10) compared with TPN alone due to increased intestinal mass (+30%, P < 0.05). GLP-2 infusion did not increase sodium-glucose cotransporter-1 mRNA abundance in fetuses or postnatal preterm pigs. Hence, the efficacy of exogenous GLP-2 to improve nutrient absorption by the intestine of fetal and preterm pigs is limited compared with term pigs and more mature animals and humans.
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Starkey, W. G., D. C. A. Candy, D. Thornber, J. Collins, A. J. Spencer, M. P. Osborne, and J. Stephen. "An in Vitro Model to Study Aspects of the Pathophysiology of Murine Rotavirus‐Induced Diarrhoea." Journal of Pediatric Gastroenterology and Nutrition 10, no. 3 (April 1990): 361–70. http://dx.doi.org/10.1002/j.1536-4801.1990.tb10012.x.
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SummaryAn in vitro system is described and validated for studying transport of solutes and water in both uninfected and rotavirus‐infected neonatal mouse intestine. Control intestine exhibited stable water absorption for periods of up to 40 min. Water absorption was temperature‐dependent, Na‐dependent, and enhanced by glucose‐containing perfusion solutions. Theophylline induced net secretion of water by control intestinal tissue. Water transport by rotavirus‐infected lower small intestine was significantly depressed as compared to control levels, and rotavirus‐infected middle small intestine exhibited net secretion of water. Upper small intestine and colon from infected animals did not differ significantly from control tissues in their ability to transport water. Water secretion by infected middle small intestine was reversed to absorption by glucose‐containing solutions.
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Chukwuma, Chika Ifeanyi, and Md Shahidul Islam. "Sorbitol increases muscle glucose uptake ex vivo and inhibits intestinal glucose absorption ex vivo and in normal and type 2 diabetic rats." Applied Physiology, Nutrition, and Metabolism 42, no. 4 (April 2017): 377–83. http://dx.doi.org/10.1139/apnm-2016-0433.
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Previous studies have suggested that sorbitol, a known polyol sweetener, possesses glycemic control potentials. However, the effect of sorbitol on intestinal glucose absorption and muscle glucose uptake still remains elusive. The present study investigated the effects of sorbitol on intestinal glucose absorption and muscle glucose uptake as possible anti-hyperglycemic or glycemic control potentials using ex vivo and in vivo experimental models. Sorbitol (2.5% to 20%) inhibited glucose absorption in isolated rat jejuna (IC50= 14.6% ± 4.6%) and increased glucose uptake in isolated rat psoas muscle with (GU50= 3.5% ± 1.6%) or without insulin (GU50= 7.0% ± 0.5%) in a concentration-dependent manner. Furthermore, sorbitol significantly delayed gastric emptying, accelerated digesta transit, inhibited intestinal glucose absorption, and reduced blood glucose increase in both normoglycemic and type 2 diabetic rats after 1 h of coingestion with glucose. Data of this study suggest that sorbitol exhibited anti-hyperglycemic potentials, possibly via increasing muscle glucose uptake ex vivo and reducing intestinal glucose absorption in normal and type 2 diabetic rats. Hence, sorbitol may be further investigated as a possible anti-hyperglycemic sweetener.
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Prager, Christiane, Heide S. Cross, and Meinrad Peterlik. "Triiodothyronine stimulates 2-deoxy-D-glucose uptake by organ cultured embryonic chick small intestine." Acta Endocrinologica 122, no. 5 (May 1990): 585–91. http://dx.doi.org/10.1530/acta.0.1220585.
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Abstract. The possible contribution of increased D-glucose absorption from the intestine to the impairment of oral glucose tolerance in hyperthyroidism was evaluated by investigating the influence of T3 on different pathways of D-glucose transport, utilizing an organ culture system of embryonic chick small intestinal explants. T3, when present in the culture medium at a concentration between 10−10-10−8 mol/l, had no effect on uptake of α-methyl-D-glucoside, but stimulated uptake of 2-deoxy-D-glucose by the intestinal epithelium in a dose-dependent fashion. T3 thereby enhanced the maximal velocity of a saturable, cytochalasin B-sensitive but phloretin-insensitive 2-deoxy-D-glucose transport system with an apparent Km of 7 mmol/l. The combined data are consistent with the assumption that T3 can enhance D-glucose entry into the intestinal epithelium through stimulationof a low-affinity transport system at the brush-border membrane of enterocytes. Our findings provide a basis for the explanation of adaptive modulation of intestinal glucose absorption in hyperthyroidism.
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Bird, A. R., W. J. Croom Jr., Y. K. Fan, L. R. Daniel, B. W. McBride, and I. L. Taylor. "Recombinant bovine somatotropin increases nutrient absorption by the proximal small intestine in sheep." Canadian Journal of Animal Science 76, no. 3 (September 1, 1996): 343–50. http://dx.doi.org/10.4141/cjas96-051.
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Dorset crossbred ewes were used to determine the effect of recombinant methionyl bovine somatotropin (bST) on small intestinal nutrient absorption. Ewes were kept indoors in individual pens and allowed free access to a concentrate diet (18% CP). (150 μg kg−1) or saline were subcutaneously injected once daily for 10 d. An in vitro assay system was used to estimate the rate of accumulation of 3H-3-O-methylglucose and 14C-proline by small intestinal segments. Feed intake and liveweight gain were similar in ewes administered bST or saline. At the end of the treatment period, plasma ST, IGF-I and glucose concentrations were significantly higher in ewes treated with bST. In the duodenum, active and total glucose absorption were greater (P < 0.05) in bST treated ewes. There was also a tendency for bST treatment to increase duodenal total proline absorption (P < 0.10). Glucose and proline absorption in the jejunum and ileum were not significantly affected by bST. Jejunal ouabain-sensitive and ouabain-insensitive oxygen consumption was similar in ewes administered saline or bST. Water, DNA and protein content of small intestinal mucosa were unaffected by bST administration. These results indicate that bST upregulates glucose transport in the duodenum of sheep. Key words: Intestine, nutrient absorption, somatotropin, IGF-I, sheep
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Dickson, J., M. Signal, D. Harris, G. Marics, P. Weston, J. Harding, P. Tóth-Heyn, J. Hómlok, B. Benyó, and J. G. Chase. "Modelling Intestinal Glucose Absorption using Continuous Glucose Monitor Data." IFAC-PapersOnLine 48, no. 20 (2015): 118–23. http://dx.doi.org/10.1016/j.ifacol.2015.10.125.
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Buddington, Randal K., Karyl K. Buddington, and Greg D. Sunvold. "Influence of fermentable fiber on small intestinal dimensions and transport of glucose and proline in dogs." American Journal of Veterinary Research 60, no. 3 (March 1, 1999): 354–58. http://dx.doi.org/10.2460/ajvr.1999.60.03.354.
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Abstract Objective To determine whether intestinal dimensions and nutrient absorption are influenced by different types of dietary fiber. Animals 10 adult Beagles of both sexes. Procedure Dogs were randomly assigned to 2 groups and fed a diet with fermentable fibers (beet pulp and oligofructose) or a nonfermentable fiber (cellulose) for 6 weeks. Effects of the diets on small intestinal dimensions were measured, and transport rates for glucose and proline were determined. Kinetics of glucose and proline uptake were defined in the proximal and middle regions of the small intestine, respectively. Results Small intestines of dogs fed fermentable fiber had 28% more nominal surface area and 37% more mucosal mass, were 35% heavier, and had 95% higher capacity for carrier-mediated glucose uptake than those of dogs fed a diet with cellulose. Differences were more pronounced in the proximal portion of the intestine. Conclusions and Clinical Relevance Diets containing fermentable fibers increase small intestinal dimensions and the capacity for nutrient absorption in dogs. These changes may reduce the risk of enteric infections or aid in treatment of intestinal diseases, particularly those involving reduced nutrient absorption.(Am J Vet Res 1999;60:354–358)
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Murr, Michel, Ken Kimura, Dan Ellsbury, Hiroaki Yoshino, Masahito Yamazato, and Robert Soper. "Absorption in the Isolated Bowel Segment." Journal of Pediatric Gastroenterology and Nutrition 17, no. 2 (August 1993): 182–85. http://dx.doi.org/10.1002/j.1536-4801.1993.tb10944.x.
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SummaryAn isolated bowel segment (IBS) is a viable amesenteric segment of intestine. This study was undertaken to investigate the effects of mesenteric vascular and neural supply on intestinal absorption. Ten rats were used for leucine absorption and another 10 for glucose absorption experiments. L‐leucine, 12 ml of 15.0 mM/L, or 3.0 mM/L of D‐glucose solution were recirculated through the IBS (n = 5) and rat jejunum that underwent sham operation (n = 5) at 2.56 ml/min for 90 min. Absorption was expressed as millimoles of leucine or glucose per gram of mucosal protein. The Student's t test was used for statistical analysis; a p ≤ 0.05 was considered significant. The net absorption of L‐leucine was 36.20 ± 3.31 mM/g of mucosal protein in the IBS and 15.52 ± 1.48 mM/g of mucosal protein in the control group (p < 0.001). The net absorption of D‐glucose was 3.82 ± 0.26 mM/g of mucosal protein in the experimental group and 4.34 ± 0.31 mM/g of mucosal protein in the control group (p = 0.02). This study concludes that absorption of leucine and glucose in the IBS is preserved after mesenteric division.
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Wielinga, Peter Y., Renate E. Wachters-Hagedoorn, Brenda Bouter, Theo H. van Dijk, Frans Stellaard, Arie G. Nieuwenhuizen, Henkjan J. Verkade, and Anton J. W. Scheurink. "Hydroxycitric acid delays intestinal glucose absorption in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 6 (June 2005): G1144—G1149. http://dx.doi.org/10.1152/ajpgi.00428.2004.
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In this study, we investigated in rats if hydroxycitric acid (HCA) reduces the postprandial glucose response by affecting gastric emptying or intestinal glucose absorption. We compared the effect of regulator HCA (310 mg/kg) and vehicle (control) on the glucose response after an intragastric or intraduodenal glucose load to investigate the role of altered gastric emptying. Steele's one-compartment model was used to investigate the effect of HCA on systemic glucose appearance after an intraduodenal glucose load, using [U-13C]-labeled glucose and d-[6,6-2H2]-labeled glucose. Because an effect on postabsorptive glucose clearance could not be excluded, the effect of HCA on the appearance of enterally administered glucose in small intestinal tissue, liver, and portal and systemic circulation was determined by [U-14C]glucose infusion. Data show that HCA treatment delays the intestinal absorption of enterally administered glucose at the level of the small intestinal mucosa in rats. HCA strongly attenuated postprandial blood glucose levels after both intragastric ( P < 0.01) and intraduodenal ( P < 0.001) glucose administration, excluding a major effect of HCA on gastric emptying. HCA delayed the systemic appearance of exogenous glucose but did not affect the total fraction of glucose absorbed over the study period of 150 min. HCA treatment decreased concentrations of [U-14C]glucose in small intestinal tissue at 15 min after [U-14C]glucose administration ( P < 0.05), in accordance with the concept that HCA delays the enteral absorption of glucose. These data support a possible role for HCA as food supplement in lowering postprandial glucose profiles.
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Thazhath, Sony S., Tongzhi Wu, Richard L. Young, Michael Horowitz, and Christopher K. Rayner. "Glucose absorption in small intestinal diseases." Expert Review of Gastroenterology & Hepatology 8, no. 3 (February 6, 2014): 301–12. http://dx.doi.org/10.1586/17474124.2014.887439.
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Bird, A. R., W. J. Croom, Y. K. Fan, B. L. Black, B. W. McBride, and I. L. Taylor. "Peptide regulation of intestinal glucose absorption." Journal of Animal Science 74, no. 10 (1996): 2523. http://dx.doi.org/10.2527/1996.74102523x.
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Atisook, K., S. Carlson, and J. L. Madara. "Effects of phlorizin and sodium on glucose-elicited alterations of cell junctions in intestinal epithelia." American Journal of Physiology-Cell Physiology 258, no. 1 (January 1, 1990): C77—C85. http://dx.doi.org/10.1152/ajpcell.1990.258.1.c77.
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Glucose alters absorptive cell tight junction structure and, as deduced from an impedance analysis model, diminishes tight junction resistance in the small intestine (J.R. Pappenheimer, J. Membr. Biol. 100: 137-148, 1987; and J.L. Madara and J.R. Pappenheimer, J. Membr. Biol. 100: 149-164, 1987). Here we provide further evidence in support of this hypothesis using the conventional approach of analysis of mucosal sheets mounted in Ussing chambers. This approach offers advantages for investigating underlying mechanisms, including the effects of ions and inhibitors on the regulation of intercellular junctions by glucose. We show that phlorizin blocks a resistance decrease elicited by glucose and demonstrate that substitution of choline for sodium also prevents the response. The dilatations in absorptive cell tight junctions that accompany this glucose-elicited response are similarly prevented by phlorizin exposure or sodium substitution. The effects of phlorizin on junctional permeability can also be demonstrated in vivo. Phlorizin reduces the transjunctional flux of creatinine in glucose-perfused intestines of anesthetized animals, even when account is taken of the reduction of fluid absorption caused by phlorizin. Last, in vivo perfusion studies suggest that although, at 25 mM luminal glucose, virtually all glucose absorption is transcellular, at a luminal glucose concentration of 125 mM approximately 30% of glucose absorption occurs paracellularly because of solvent drag across tight junctions of altered permeability.(ABSTRACT TRUNCATED AT 250 WORDS)
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Kim, Hye Kyung. "Ecklonia cavaInhibits Glucose Absorption and Stimulates Insulin Secretion in Streptozotocin-Induced Diabetic Mice." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/439294.
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Aims of study. Present study investigated the effect ofEcklonia cava(EC) on intestinal glucose uptake and insulin secretion.Materials and methods. Intestinal Na+-dependent glucose uptake (SGU) and Na+-dependent glucose transporter 1 (SGLT1) protein expression was determined using brush border membrane vesicles (BBMVs). Glucose-induced insulin secretion was examined in pancreatic β-islet cells. The antihyperglycemic effects of EC, SGU, and SGLT1 expression were determined in streptozotocin (STZ)-induced diabetic mice.Results. Methanol extract of EC markedly inhibited intestinal SGU of BBMV with the IC50value of 345 μg/mL. SGLT1 protein expression was dose dependently down regulated with EC treatment. Furthermore, insulinotrophic effect of EC extract was observed at high glucose media in isolated pancreatic β-islet cellsin vitro. We next conducted the antihyperglycemic effect of EC in STZ-diabetic mice. EC supplementation markedly suppressed SGU and SGLT1 abundance in BBMV from STZ mice. Furthermore, plasma insulin level was increased by EC treatment in diabetic mice. As a result, EC supplementation improved postprandial glucose regulation, assessed by oral glucose tolerance test, in diabetic mice.Conclusion. These results suggest that EC play a role in controlling dietary glucose absorption at the intestine and insulinotrophic action at the pancreas contributing blood glucose homeostasis in diabetic condition.
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Singh, Shailendra Vikram Jitendra, Dharmaraja Meetei Usham, Subhalakshmi Devi Akham, and Rita Devi Sanjenbam. "Effect of ethyl acetate extract of Melothria perpusilla on intestinal absorption of glucose in albino rats." International Journal of Basic & Clinical Pharmacology 6, no. 3 (February 24, 2017): 543. http://dx.doi.org/10.18203/2319-2003.ijbcp20170539.
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Background: Diabetes mellitus is a spectrum of conditions that includes hyperglycemia. Safety issues limit the optimal use of anti diabetic drugs. The objectives of the study were to evaluate the effect of ethyl acetate extract of Melothria perpusilla (EAEMP) on intestinal absorption of glucose in albino rats.Methods: Twenty four healthy albino rats were divided into four groups (control, standard, test I and test II) of six animals each weighing between 120-150g. Animals in control group were fed with 2% gum acacia, standard group with metformin 150mg/kg, test I with 250mg/kg of EAEMP and test II with 500mg/kg of EAEMP. After treatment for seven days, rats were fasted overnight. Intestinal loop of 10 cm from the pyloric end was prepared, keeping the blood supply intact under anaesthesia. One ml of 250mg% D-glucose in normal saline was injected in the lumen of loop. Rats were sacrificed and the loop was removed after 15minutes. Weight of excised loop was measured and fluid was recovered. The glucose absorbed was calculated by the difference between the amount introduced and recovered after the absorptive period. After dehydrating, the dry weight of the tissue segment was measured. Intestinal glucose absorption was expressed in mg/g dry weight tissue/h.Results: The non parametric data were analysed by Kruskal Wallis test. Ethyl acetate extract of Melothria perpusilla produced a significant reduction in intestinal glucose absorption when compared with control and standard.Conclusions: Treatment with Melothria perpusilla inhibits intestinal glucose absorption probably by inhibition of flavonoids on Na+-K+ATPase.
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Trotta, Ronald J., David L. Harmon, James C. Matthews, and Kendall C. Swanson. "Nutritional and Physiological Constraints Contributing to Limitations in Small Intestinal Starch Digestion and Glucose Absorption in Ruminants." Ruminants 2, no. 1 (December 23, 2021): 1–26. http://dx.doi.org/10.3390/ruminants2010001.
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Increased efficiency of nutrient utilization can potentially be gained with increased starch digestion in the small intestine in ruminants. However, ruminants have quantitative limits in the extent of starch disappearance in the small intestine. The objective is to explore the nutritional and physiological constraints that contribute to limitations of carbohydrate assimilation in the ruminant small intestine. Altered digesta composition and passage rate in the small intestine, insufficient pancreatic α-amylase and/or small intestinal carbohydrase activity, and reduced glucose absorption could all be potentially limiting factors of intestinal starch assimilation. The absence of intestinal sucrase activity in ruminants may be related to quantitative limits in small intestinal starch hydrolysis. Multiple sequence alignment of the sucrase-isomaltase complex gives insight into potential molecular mechanisms that may be associated with the absence of intestinal sucrase activity, reduced capacity for intestinal starch digestion, and limitations in the efficiency of feed utilization in cattle and sheep. Future research efforts in these areas will aid in our understanding of small intestinal starch digestion and glucose absorption to optimize feeding strategies for increased meat and milk production efficiency.
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Pal, Atanu, David B. Rhoads, and Ali Tavakkoli. "Portal milieu and the interplay of multiple antidiabetic effects after gastric bypass surgery." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 5 (May 1, 2019): G668—G678. http://dx.doi.org/10.1152/ajpgi.00389.2018.
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Diabetes is a worldwide health problem. Roux-en-Y gastric bypass (RYGB) leads to rapid resolution of type 2 diabetes (T2D). Decreased hepatic insulin resistance is key, but underlying mechanisms are poorly understood. We hypothesized that changes in intestinal function and subsequent changes in portal venous milieu drive some of these postoperative benefits. We therefore aimed to evaluate postoperative changes in portal milieu. Two rat strains, healthy [Sprague-Dawley (SD)] and obese diabetic [Zucker diabetic fatty (ZDF)] rats, underwent RYGB or control surgery. After 4 wk, portal and systemic blood was sampled before and during an intestinal glucose bolus to investigate changes in intestinal glucose absorption (Gabsorp) and utilization (Gutil), and intestinal secretion of incretins and glucagon-like peptide-2 (GLP-2). Hepatic activity of dipeptidyl peptidase-4 (DPP4), which degrades incretins, was also measured. RYGB decreased Gabsorp in both rat strains. Gutil increased in SD rats and decreased in ZDF rats. In both strains, there was increased expression of intestinal hexokinase and gluconeogenesis enzymes. Systemic incretin and GLP-2 levels also increased after RYGB. This occurred without an increase in secretion. Hepatic DPP4 activity and expression were unchanged. RYGB perturbs multiple intestinal pathways, leading to decreased intestinal glucose absorption and increased incretin levels in both healthy and diabetic animals. In diabetic rats, intestinal glucose balance shifts toward glucose release. The portal vein as the gut-liver axis may integrate these intestinal changes to contribute to rapid changes in hepatic glucose and hormone handling. This fresh insight into the surgical physiology of RYGB raises the hope of less invasive alternatives. NEW & NOTEWORTHY Portal milieu after gastric bypass surgery is an underinvestigated area. Roux-en-Y gastric bypass perturbs multiple intestinal pathways, reducing intestinal glucose absorption and increasing incretin levels. In diabetic rats, the intestine becomes a net releaser of glucose, increasing portal glucose levels. The portal vein as the gut-liver axis may integrate these intestinal changes to contribute to changes in hepatic glucose handling. This fresh insight raises the hope of less invasive alternatives.
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Rtibi, Kais, Slimen Selmi, Rafik Balti, Lamjed Marzouki, and Hichem Sebai. "Natural Bioactive Compounds with Small-Bowel Glucose/Antiabsorption and Sugar Digestion Enzymes’ Inhibition Actions: New Strategy to Relieve Hyperglycemia and Diabetes." Recent Advances in Biology and Medicine 5 (2019): 1. http://dx.doi.org/10.18639/rabm.2019.879443.
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Intestinal glucose absorption/inhibition activity by natural bioactive compounds is considered a new strategy for prevention/treatment of uncontrolled hyperglycemia and diabetes as well as chronic human metabolic disorders. This mini review provides scientific evidence of the contribution of natural bioactive nutrients to inhibit glucose absorption in the small bowel. Many studies were realized on intestinal glucose transport in vitro and on postprandial glucose levels in vivo. In this context, the main designated constituents are (+)-catechin, (-)-epicatechin, (-)-epigallocatechin, epicatechingallate, tannic acid, resveratrol, and chlorogenic acid. The therapeutic approaches are to retard the absorption of glucose by inhibition of carbohydrate-hydrolyzing enzymes such as intestinal glycosidases (α-amylase and α-glycosidase) and the inhibition of intestinal Na+-dependent glucose absorption mediated by reduced expression of glucose transporter (SGLT1). These studies revealed that natural bioactive compounds, as potential candidates, can be designed as natural products for the development of novel functional foods or nutraceuticals to relieve hyperglycemia/diabetes.
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Croom Jr, W. James, Brian McBride, Anthony R. Bird, Yang-Kwang Fan, Jack Odle, Mark Froetschel, and Ian L. Taylor. "Regulation of intestinal glucose absorption: A new issue in animal science." Canadian Journal of Animal Science 78, no. 1 (March 1, 1998): 1–13. http://dx.doi.org/10.4141/a97-056.
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Intestinal glucose absorption occurs via Na+-dependent glucose cotransporters (SGLT1) located in the luminal membrane of enterocytes and is driven by an electrochemical gradient maintained by Na+/K+ ATPase located on the basolateral membrane. Twenty percent of whole animal energy expenditures can be accounted for by the gastrointestinal tract, most of which is the result of Na+/K+ ATPase function. Active intestinal glucose transport is regulated by a number of gastrointestinal peptides such as epidermal growth factor (EGF) and peptide YY (PYY). PYY and EGF can upregulate intestinal glucose absorption by as much as 200–300%. Of special interest is the fact that the energetic costs of intestinal tissue function can vary in relationship to the amount of glucose transported. This value termed "apparent energetic efficiency of glucose uptake" (APEE) may be of value in evaluating the energetic costs of glucose and other nutrients during various physiological and nutritional states. Recent studies suggest that intensive genetic selection for production traits in poultry may result in intestinal absorption being rate-limiting for full phenotypic expression of these traits. Further research is needed to clarify this issue. Key words: Glucose absorption, intestinal, energy metabolism, peptides, genetic selection
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Brouwer, I. A., A. G. Lemmens, and A. C. Beynenl. "Dietary fructose v. glucose lowers ferrous-iron absorption in rats." British Journal of Nutrition 70, no. 1 (July 1993): 171–78. http://dx.doi.org/10.1079/bjn19930114.
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The effect of dietary fructose v. glucose on Fe solubility in the small intestine and apparent Fe absorption was studied in rats. Female rats were fed for 4 weeks on low-Fe (10 mg Fe/kg) or normal-Fe (40 mg Fe/kg) diets containing either fructose or glucose (709·4 g monosaccharide/kg). Fe was added to the diets in the form of FeSO4. The low-Fe diets did not lower levels of haemoglobin and packed cell volume, but significantly lowered Fe concentration and Fe mass in the liver, kidney and spleen. Fructose v. glucose also lowered Fe concentrations in these organs, but did not alter absolute Fe contents. Low Fe intake reduced the amount of Fe in the intestinal lumen. The total amount of Fe and Fe concentration in the liquid phase of the proximal intestinal lumen were depressed by fructose irrespective of Fe intake. Fructose also lowered the amount of Fe in the liquid phase of the distal intestine. In keeping with these observations, dietary fructose significantly lowered apparent absorption of Fe at the two levels of Fe intake. Decreasing the intake of Fe raised the percentage of apparent Fe absorption.
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Carroll, K. M., R. J. Wood, E. B. Chang, and I. H. Rosenberg. "Glucose enhancement of transcellular calcium transport in the intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 3 (September 1, 1988): G339—G345. http://dx.doi.org/10.1152/ajpgi.1988.255.3.g339.
Full textAbstract:
Glucose stimulates calcium transport in vitro in rat duodenal tissue and isolated enterocytes. Under short-circuited conditions, glucose increased mucosal to serosal calcium flux (JCa(m----s)) without altering serosal to mucosal calcium flux (JCa(s----m)) in the duodenum, the primary site of active calcium absorption in the rat small intestine. The half-maximal dose (ED50) of the glucose stimulatory effect was less than 1 mM, and an increase in JCa(m----s) of 80% over control was seen at a glucose concentration of 50 mM. Glucose did not increase calcium flux in the ileum where active calcium absorption is minimal. Glucose stimulated net calcium uptake by 35% in isolated duodenal enterocytes. Glucose did not alter calcium efflux from preloaded enterocytes suspended in calcium-free buffer. Glucose enhancement of net calcium uptake in enterocytes was not caused by altered cell membrane integrity or functional viability. The nonmetabolizable glucose analogue alpha-methylglucoside did not stimulate calcium transport. Our findings suggest that glucose can stimulate intestinal calcium absorption, at least partially, by enhancing transcellular calcium transport and that cellular glucose metabolism is necessary for stimulation of this route of calcium transport.
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Yakovleva, L. M., S. V. Lezhenina, Zh V. Maslova, and S. V. Kupriyanov. "Study of the absorptive intestinal function in an experimental model of chronic alcohol intoxication." Kazan medical journal 93, no. 3 (June 15, 2012): 499–502. http://dx.doi.org/10.17816/kmj1877.
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Aim. To study the absorptive function of the rat intestine on the background of prolonged alcohol intoxication. Methods. The study was performed on 24 nonlinear white male rats (12 animals in the control and experimental groups) weighing 220-240 g, which had a daily consumption of 20° ethanol solution (ethyl alcohol) for the duration of 180 days. After 6 months perfusion of the isolated segment of jejunum with a dextrose (glucose) solution 35 mmol/L was performed by in the rats the method A.M. Ugolev. The luminescence-histochemical method was used to examine the content of catecholamines and serotonin in the neuroamine containing structures. Results. In the control rats, the rate of absorption in the first 10 min of perfusion reached a maximum value with a further decrease in the intensity of absorption. The content of serotonin and catecholamines in the absorptive epithelial layer of the jejunal villi was lower than in the muscle membrane. In the experimental rats the content of biogenic amines in the wall of the jejunum increased: the amount of serotonin in the absorptive layer of the villi increased up to 122% and in the muscle membrane - up to 126%. The content of catecholamines also increased up to 154% in the muscle membrane and up to 124% in the epithelial layer in the area of the villi compared with controls. In conditions of chronic alcohol intoxication the rate of absorption of dextrose (glucose) during perfusion in the first 30 minutes was reduced by 33% compared with the control. During the next hour, the intensity of absorption reduced by 45% (55% of control). After 1.5 hours the absorption increased slightly, accounting for 64% of the control value and by the end of the 2nd hour the intensity of the absorption reached 91%. Conclusion. An increase in content of catecholamines and serotonin in the mucous and muscular layers of the intestine in chronic alcohol intake and a decrease in the intensity of the absorption of dextrose (glucose) was established; in the setting if modified combined effects of neurotransmitters on smooth muscle cells an increased motor effect is formed, which is accompanied by rapid evacuation of the intestinal chyme with a reduction in the rate of absorption
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Scholtka, B., F. Stümpel, and K. Jungermann. "Acute increase, stimulated by prostaglandin E2, in glucose absorption via the sodium dependent glucose transporter-1 in rat intestine." Gut 44, no. 4 (April 1, 1999): 490–96. http://dx.doi.org/10.1136/gut.44.4.490.
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BACKGROUND/AIMSAcute stimulation by cAMP of the sodium dependent glucose cotransporter SGLT1 has previously been shown. As prostaglandin E2(PGE2) increases intracellular cAMP concentrations via its receptor subtypes EP2R and EP4R, it was investigated whether PGE2 could enhance intestinal glucose absorption.METHODSThe action of PGE2 on carbohydrate absorption in the ex situ perfused rat small intestine and on 3-O-[14C]methylglucose uptake in isolated villus tip enterocytes was determined. Expression of mRNA for the PGE2 receptor subtypes 1–4 was assayed in enterocytes by reverse transcriptase polymerase chain reaction (RT-PCR).RESULTSIn the perfused small intestine, PGE2 acutely increased absorption of glucose and galactose, but not fructose (which is not a substrate for SGLT1); in isolated enterocytes it stimulated 3-O-[14C]methylglucose uptake. The 3-O-[14C]methylglucose uptake could be inhibited by the cAMP antagonist RpcAMPS and the specific inhibitor of SGLT1, phlorizin. High levels of EP2R mRNA and EP4R mRNA were detected in villus tip enterocytes.CONCLUSIONPGE2acutely increased glucose and galactose absorption by the small intestine via the SGLT1, with cAMP serving as the second messenger. PGE2 acted directly on the enterocytes, as the stimulation was still observed in isolated enterocytes and RT-PCR detected mRNA for the cAMP-increasing PGE2 receptors EP2R and EP4R.
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Patra, F. C., A. S. M. Hamidur Rahman, M. A. Wahed, and K. A. Al‐Mahmud. "Enhanced Sodium Absorption by Citrate." Journal of Pediatric Gastroenterology and Nutrition 11, no. 3 (October 1990): 385–88. http://dx.doi.org/10.1002/j.1536-4801.1990.tb10131.x.
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SummaryThe effect of citrate on sodium, potassium chloride, and water absorption in the presence of glucose from the whole rat small intestine was studied by an in vivo marker perfusion technique. The perfusion solutions contained glucose and were similar in their electrolyte composition to the currently recommended oral rehydration solution for the treatment and prevention of diarrheal dehydration. Significantly more sodium and water absorption occurred from the citrate‐containing solution than from the one without citrate. It is concluded that citrate enhances net sodium absorption from a glucose electrolyte solution in the rat small intestine independent of glucose‐stimulated absorption.
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Mangino, M. J., and C. C. Chou. "Thromboxane synthesis inhibition and postprandial intestinal hyperemia and oxygenation." American Journal of Physiology-Gastrointestinal and Liver Physiology 250, no. 1 (January 1, 1986): G64—G69. http://dx.doi.org/10.1152/ajpgi.1986.250.1.g64.
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The effects of imidazole and U-63557A (Upjohn), inhibitors of thromboxane synthesis, on food-induced changes in intestinal blood flow and oxygen uptake were determined in the jejunum of anesthetized dogs. Intra-arterial (5.0 mg/min ia) infusions of imidazole had no effect on the postprandial intestinal hyperemia but significantly potentiated food-induced increases in oxygen uptake via enhanced oxygen extraction. Furthermore, imidazole had no effect on intestinal glucose absorption. The selective thromboxane synthesis inhibitor U-63557A (5 mg/kg iv) also enhanced oxygen uptake during nutrient absorption and had no effect on the hyperemia or glucose absorption. Our study indicates that inhibition of thromboxane synthesis has no effect on either resting intestinal blood flow or postprandial intestinal hyperemia but significantly enhances postprandial oxygen extraction and uptake. The potentiation of the food-induced increases in oxygen uptake by imidazole and U-63557A appears not to be related to glucose absorption. Endogenous thromboxane therefore appears to inhibit oxygen uptake more than blood flow, and yet does not affect glucose absorption during nutrient absorption.
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Aoki, Kai, Takuji Suzuki, Fang Hui, Takuro Nakano, Koki Yanazawa, Masato Yonamine, Shinichiro Fujita, et al. "Acute Low-Intensity Treadmill Running Upregulates the Expression of Intestinal Glucose Transporters via GLP-2 in Mice." Nutrients 13, no. 5 (May 20, 2021): 1735. http://dx.doi.org/10.3390/nu13051735.
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The effects of exercise on nutrient digestion and absorption in the intestinal tract are not well understood. A few studies have reported that exercise training increases the expression of molecules involved in carbohydrate digestion and absorption. Exercise was also shown to increase the blood concentration of glucagon-like peptide-2 (GLP-2), which regulates carbohydrate digestion and absorption in the small intestine. Therefore, we investigated the effects of exercise on the expression of molecules involved in intestinal digestion and absorption, including GLP-2. Six-week-old male mice were divided into a sedentary (SED) and low-intensity exercise (LEx) group. LEx mice were required to run on a treadmill (12.5 m/min, 1 h), whereas SED mice rested. All mice were euthanized 1 h after exercise or rest, and plasma, jejunum, ileum, and colon samples were collected, followed by analysis via IHC, EIA, and immunoblotting. The levels of plasma GLP-2 and the jejunum expression of the GLP-2 receptor, sucrase-isomaltase (SI), and glucose transporter 2 (GLUT2) were higher in LEx mice. Thus, we showed that acute low-intensity exercise affects the expression of molecules involved in intestinal carbohydrate digestion and absorption via GLP-2. Our results suggest that exercise might be beneficial for small intestine function in individuals with intestinal frailty.