Relevant bibliographies by topics / Gastrointestinal hormones Physiology

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Academic literature on the topic 'Gastrointestinal hormones Physiology'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Gastrointestinal hormones Physiology"

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REHFELD, JENS F. "The New Biology of Gastrointestinal Hormones." Physiological Reviews 78, no. 4 (October 1, 1998): 1087–108. http://dx.doi.org/10.1152/physrev.1998.78.4.1087.

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Rehfeld, Jens F. The New Biology of Gastrointestinal Hormones. Physiol. Rev. 78: 1087–1108, 1998. — The classic concept of gastrointestinal endocrinology is that of a few peptides released to the circulation from endocrine cells, which are interspersed among other mucosal cells in the upper gastrointestinal tract. Today more than 30 peptide hormone genes are known to be expressed throughout the digestive tract, which makes the gut the largest endocrine organ in the body. Moreover, development in cell and molecular biology now makes it feasible to describe a new biology for gastrointestinal hormones based on five characteristics. 1) The structural homology groups the hormones into families, each of which is assumed to originate from a common ancestral gene. 2) The individual hormone gene is often expressed in multiple bioactive peptides due to tandem genes encoding different hormonal peptides, alternative splicing of the primary transcript, or differentiated processing of the primary translation product. By these mechanisms, more than 100 different hormonally active peptides are produced in the gastrointestinal tract. 3) In addition, gut hormone genes are widely expressed, also outside the gut. Some are expressed only in neuroendocrine cells, whereas others are expressed in a multitude of different cells, including cancer cells. 4) The different cell types often express different products of the same gene, “cell-specific expression.” 5) Finally, gastrointestinal hormone-producing cells release the peptides in different ways, so the same peptide may act as an acute blood-borne hormone, as a local growth factor, as a neurotransmitter, and as a fertility factor. The new biology suggests that gastrointestinal hormones should be conceived as intercellular messengers of general physiological impact rather than as local regulators of the upper digestive tract.
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Lucas, Alan, Stephen R. Bloom, and Albert Aynsley Green. "Gastrointestinal peptides and the adaptation to extrauterine nutrition." Canadian Journal of Physiology and Pharmacology 63, no. 5 (May 1, 1985): 527–37. http://dx.doi.org/10.1139/y85-092.

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The adaptation to extrauterine nutrition involves complex physiological changes at birth which may be regulated by genetic endowment; enteral nutrients, secretions, and bacteria; and endogenous hormones and exogenous hormones in breast milk. The hypothesis is explored that enteral feeding after birth may trigger key adaptations in the gut and in metabolism partly through the mediation of gastrointestinal hormone secretion. Gut peptides are found in the early human fetal gut and by the second trimester some are found in high concentrations in the fetal circulation and amniotic fluid. Major plasma hormonal surges occur during the neonatal period in term and preterm infants: notably in enteroglucagon, gastrin, motilin, neurotensin, gastrointestinal peptide, and pancreatic polypeptide. These events do not occur in neonates deprived of enteral feeding. A progressive development of dynamic gut hormonal responses to feeding is observed. The pattern of gut endocrine changes after birth is influenced by the type and route of feeding. Potential pathophysiological effects of depriving high risk neonates of enteral feeding are considered. It is speculated that infants committed to prolonged total parenteral nutrition from birth may benefit from the biological effects of intraluminal nutrients used in subnutritional quantities.
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Cullen, Joseph J., J. Chris Eagon, and Keith A. Kelly. "Gastrointestinal peptide hormones during postoperative ileus." Digestive Diseases and Sciences 39, no. 6 (June 1994): 1179–84. http://dx.doi.org/10.1007/bf02093781.

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Premen, A. J., P. R. Kvietys, and D. N. Granger. "Postprandial regulation of intestinal blood flow: role of gastrointestinal hormones." American Journal of Physiology-Gastrointestinal and Liver Physiology 249, no. 2 (August 1, 1985): G250—G255. http://dx.doi.org/10.1152/ajpgi.1985.249.2.g250.

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Systemic arterial pressure, jejunal perfusion pressure, and jejunal blood flow were measured in eight autoperfused canine jejunum preparations (5 dogs) before and during local intra-arterial infusion of physiological doses of secretin (18.5 pM), neurotensin (233 pM), and cholecystokinin octapeptide (CCK-8, 30 pM). Intra-arterial infusion of secretin, neurotensin, or CCK-8 alone did not affect either systemic or jejunal arterial pressures. Likewise, jejunal blood flow was not significantly altered by secretin (3 +/- 3%), neurotensin (-5 +/- 4%), or CCK-8 (-5 +/- 5%). Even when all three hormones were infused simultaneously, jejunal blood flow was not altered (2 +/- 3%). However, when infused at rates that produced calculated arterial blood levels some 100 times greater than those reported as “postprandial,” each hormone alone, as well as in combination, produced marked increases in jejunal blood flow. Secretin, neurotensin, and CCK-8 increased blood flow by 34 +/- 8, 31 +/- 11, and 24 +/- 5%, respectively. Simultaneous infusion of all three hormones increased jejunal blood flow by 47 +/- 11%. These data suggest that, either alone or in combination, secretin, neurotensin, and CCK-8 are not of quantitative importance in regulating jejunal blood flow during the postprandial state. However, higher (presumably pharmacological) blood levels of these hormones do significantly elevate jejunal blood flow.
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Lu, Van B., Fiona M. Gribble, and Frank Reimann. "Nutrient-Induced Cellular Mechanisms of Gut Hormone Secretion." Nutrients 13, no. 3 (March 9, 2021): 883. http://dx.doi.org/10.3390/nu13030883.

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The gastrointestinal tract can assess the nutrient composition of ingested food. The nutrient-sensing mechanisms in specialised epithelial cells lining the gastrointestinal tract, the enteroendocrine cells, trigger the release of gut hormones that provide important local and central feedback signals to regulate nutrient utilisation and feeding behaviour. The evidence for nutrient-stimulated secretion of two of the most studied gut hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), along with the known cellular mechanisms in enteroendocrine cells recruited by nutrients, will be the focus of this review. The mechanisms involved range from electrogenic transporters, ion channel modulation and nutrient-activated G-protein coupled receptors that converge on the release machinery controlling hormone secretion. Elucidation of these mechanisms will provide much needed insight into postprandial physiology and identify tractable dietary approaches to potentially manage nutrition and satiety by altering the secreted gut hormone profile.
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Somogyi, V., A. Gyorffy, T. J. Scalise, D. S. Kiss, G. Goszleth, T. Bartha, V. L. Frenyo, and A. Zsarnovszky. "Endocrine factors in the hypothalamic regulation of food intake in females: a review of the physiological roles and interactions of ghrelin, leptin, thyroid hormones, oestrogen and insulin." Nutrition Research Reviews 24, no. 1 (March 22, 2011): 132–54. http://dx.doi.org/10.1017/s0954422411000035.

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Controlling energy homeostasis involves modulating the desire to eat and regulating energy expenditure. The controlling machinery includes a complex interplay of hormones secreted at various peripheral endocrine endpoints, such as the gastrointestinal tract, the adipose tissue, thyroid gland and thyroid hormone-exporting organs, the ovary and the pancreas, and, last but not least, the brain itself. The peripheral hormones that are the focus of the present review (ghrelin, leptin, thyroid hormones, oestrogen and insulin) play integrated regulatory roles in and provide feedback information on the nutritional and energetic status of the body. As peripheral signals, these hormones modulate central pathways in the brain, including the hypothalamus, to influence food intake, energy expenditure and to maintain energy homeostasis. Since the growth of the literature on the role of various hormones in the regulation of energy homeostasis shows a remarkable and dynamic expansion, it is now becoming increasingly difficult to understand the individual and interactive roles of hormonal mechanisms in their true complexity. Therefore, our goal is to review, in the context of general physiology, the roles of the five best-known peripheral trophic hormones (ghrelin, leptin, thyroid hormones, oestrogen and insulin, respectively) and discuss their interactions in the hypothalamic regulation of food intake.
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Jordinson, Mark, Robert A. Goodlad, Audrey Brynes, Philip Bliss, Mohammad A. Ghatei, Stephen R. Bloom, Anthony Fitzgerald, et al. "Gastrointestinal responses to a panel of lectins in rats maintained on total parenteral nutrition." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 5 (May 1, 1999): G1235—G1242. http://dx.doi.org/10.1152/ajpgi.1999.276.5.g1235.

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Total parenteral nutrition (TPN) causes atrophy of gastrointestinal epithelia, so we asked whether lectins that stimulate epithelial proliferation can reverse this effect of TPN. Two lectins stimulate pancreatic proliferation by releasing CCK, so we asked whether lectins that stimulate gastrointestinal proliferation also release hormones that might mediate their effects. Six rats per group received continuous infusion of TPN and a once daily bolus dose of purified lectin (25 mg ⋅ rat−1 ⋅ day−1) or vehicle alone (control group) for 4 days via an intragastric cannula. Proliferation rates were estimated by metaphase arrest, and hormones were measured by RIAs. Phytohemagglutinin (PHA) increased proliferation by 90% in the gastric fundus ( P < 0.05), doubled proliferation in the small intestine ( P < 0.001), and had a small effect in the midcolon ( P< 0.05). Peanut agglutinin (PNA) had a minor trophic effect in the proximal small intestine ( P < 0.05) and increased proliferation by 166% in the proximal colon ( P < 0.001) and by 40% in the midcolon ( P < 0.001). PNA elevated circulating gastrin and CCK by 97 ( P< 0.05) and 81% ( P < 0.01), respectively, and PHA elevated plasma enteroglucagon by 69% and CCK by 60% (both P < 0.05). Only wheat germ agglutinin increased the release of glucagon-like peptide-1 by 100% ( P < 0.05). PHA and PNA consistently reverse the fall in gastrointestinal and pancreatic growth associated with TPN in rats. Both lectins stimulated the release of specific hormones that may have been responsible for the trophic effects. It is suggested that lectins could be used to prevent gastrointestinal atrophy during TPN. Their hormone-releasing effects might be involved.
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Liddle, R. A. "Regulation of cholecystokinin secretion by intraluminal releasing factors." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 3 (September 1, 1995): G319—G327. http://dx.doi.org/10.1152/ajpgi.1995.269.3.g319.

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Ingested nutrients stimulate secretion of gastrointestinal hormones that are necessary for the coordinated processes of digestion and absorption of food. One of the most important hormonal regulators of the digestive process is cholecystokinin (CCK). This hormone is concentrated in the proximal small intestine and is secreted into the blood on the ingestion of proteins and fats. The physiological actions of CCK include stimulation of pancreatic secretion and gallbladder contraction, regulation of gastric emptying, and induction of satiety. Therefore, in a highly coordinated manner CCK regulates the ingestion, digestion, and absorption of nutrients. The manner by which foods affect enteric hormone secretion is largely unknown. However, it has recently become apparent that two CCK-releasing factors are present in the lumen of the proximal small intestine. One of these factors, known as monitor peptide, has been chemically characterized. Monitor peptide is produced by pancreatic acinar cells and is secreted by way of the pancreatic duct into the duodenum. On reaching the small intestine, monitor peptide interacts with CCK cells to induce hormone secretion. A CCK-releasing factor of intestinal origin has been partially characterized and is responsible for stimulation of CCK secretion after 1) ingestion of protein or fats, 2) instillation of protease inhibitors into the duodenum, or 3) diversion of bile-pancreatic juice from the upper small intestine. Together, these releasing factors provide positive and negative feedback mechanisms for regulation of CCK secretion. This review discusses the physiological observations that have led to the chemical characterization of the CCK-releasing factors and the potential implications of this work to other hormones of the gastrointestinal tract.
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Mandal, Anwesha, Kedar S. Prabhavalkar, and Lokesh K. Bhatt. "Gastrointestinal hormones in regulation of memory." Peptides 102 (April 2018): 16–25. http://dx.doi.org/10.1016/j.peptides.2018.02.003.

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Dockray, Graham J. "Gastrointestinal hormones and the dialogue between gut and brain." Journal of Physiology 592, no. 14 (March 17, 2014): 2927–41. http://dx.doi.org/10.1113/jphysiol.2014.270850.

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Dissertations / Theses on the topic "Gastrointestinal hormones Physiology"

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Vogel, Lee. "Characterization of rat intestinal immunoreactive motilin (IR-M)." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26658.

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Interdigestive myoelectric activity in rat intestine has been recorded and characterized. The interdigestive pattern of activity can be disrupted by oral glucose and high doses of the duodenal ulcerogen cysteamine. Intravenous glucose had no effect on the interdigestive myoelectric pattern, nor did high doses of porcine motilin. Attempts were made to develop a hybridoma cell line secreting antibodies that would recognize rat Intestinal immunoreactive motilin (IR-M). The murine myeloma cell line NS1 was fused with murine B-cells primed against porcine motilin. One hundred of the monoclonal cell lines produced secreted monoclonal antibodies that recognized porcine motilin. Attempts to identify a cell line secreting antibodies with the ability to stain rat intestinal tissue, however, produced only negative results. Rat intestinal IR-M has been characterized with respect to immunocytochemistry (ICC), radioimmunoassay (RIA), and chromatographic properties. The biological activity of partially purified rat intestinal IR-M has also been evaluated utilizing a rabbit isolated duodenal muscle strip preparation. Five different antisera and one monoclonal antibody directed against natural porcine motilin were utilized in an effort to detect IR-M containing cells in rat intestinal tissues. A variety of techniques were employed including tissue fixation with either Bouins, paraformaldehyde, or benzoquinone. In addition a variety of staining methods including, fluorescein conjugated second antibody, peroxidase-antiperoxidase or peroxidase conjugated second antibody techniques were used. All methods using these antibodies failed to detect IR-H in the rat small intestine. Porcine motilin was able to displace ¹²⁵I-motilin from antisera 13-3, 72X and M03. These antisera were utilized in a motilin RIA to evaluate acid extracts of rat intestinal tissue for IR-M. Only antisera 13-3 and 72X were capable of detecting IR-M in gut extracts, and these antisera gave different distributions of IR-M In the proximal small bowel. Rat intestinal tissue was extracted into 2% trifluoroacetic acid and the soluble fraction clarified by centrifugation. This acid extracted material was precipitated with sodium chloride then dissolved in methanol at pH 6.0. Methanol soluble material was precipitated with ether and the ether precipitate then dissolved in water and chromatographed on Sep-Pak C₁₈ cartridges (Waters). Sep-Pak cartridges were eluted with 50% acetonitrile: 0.1% TFA. The 50% eluate was then fractionated further using cation exchange, gel filtration and reverse phase high pressure liquid chromatography (HPLC). Rat intestinal IR-M peaks from cation exchange chromatography on SP-Sephadex-C25 (Pharmacia) were concentrated and examined for contractility in a rabbit duodenal muscle strip preparation. Purification after SP-Sephadex-C25 was approximately 20 fold. Desensitization of rabbit duodenum to porcine motilin could be demonstrated by pre-treatment with motilin. Contractile activity of partially purified rat intestinal IR-M was not inhibited by pretreatment with motilin. Chromatography on Bio-Gel P-10 (Biorad) eluted with 0.2M acetic HPLC, using a linear gradient of water/acetonitrile (10-45% acetonitrile in 30 min), rat intestinal IR-M did not co-elute with natural porcine motilin. In conclusion, the molecular weight of rat intestinal IR-M appeared to be similar to porci ne motilin as these two substances demonstrated co-elution on gel permeation chromatography. The lack of co-elution with porcine motilin on HPLC indicates that other molecular characteristics of rat intestinal IR-M, such as hydrophobicity, are not similar to porcine motilin. Furthermore, partially purified rat intestinal IR-M did induce a contractile response in rabbit duodenal muscle strips but porcine motilin did not desensitize this preparation to the contractile activity of rat intestinal extracts. This suggests that the contractile activity of these two compounds is induced via different receptor mechanisms. It is concluded that the immunoreactive motilin found in rat intestinal extracts does not resemble natural porcine motilin in structure or biological activity.<br>Medicine, Faculty of<br>Cellular and Physiological Sciences, Department of<br>Graduate
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Lemmey, Andrew Bruce. "Effects of insulin-like growth factors (IGFS) on recovery from gut resection in rats : a thesis submitted to the University of Adelaide, South Australia for the degree of Doctor of Philosophy." 1992, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phl554.pdf.

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Includes bibliographical references (leaves 159-213) Shows that IGF-I peptides are effective in diminishing post-surgical catabolism and enhancing adaptive gut hyperplasia in rats recovering from massive small bowel resection.
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Gillard, Laura. "Mécanismes de l'adaptation physiopathologique au cours du syndrome de grêle court : étude chez le rat et l'homme." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC150.

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Le syndrome du grêle court (SGC) est consécutif à une résection intestinale étendue, principale cause d'insuffisance intestinale, dont le traitement est la nutrition parentérale (NP). En présence d'une partie ou de la totalité du côlon dans la continuité de l'intestin grêle, une adaptation s'installe et permet de diminuer voire de sevrer le patient de la NP. Cette adaptation est caractérisée par des changements morpho-fonctionnels de l'épithélium intestinal résiduel, par l'apparition d'une hyperphagie chez 70% des patients, et par une dysbiose du microbiote intestinal. Le but de ce travail est de mieux comprendre les mécanismes moléculaires, cellulaires et microbiologiques de l'adaptation physiopathologique dans le SGC. Nous avons mis au point 2 modèles de résection intestinale chez le rat mimant le SGC (IR) en montage digestif en anastomose jéjuno-colique (JC) et jéjuno-iléale (JI). Nous montrons pour la première fois, chez le rat IR JC, une augmentation de l'expression de neuropeptides orexigènes (NPY, AgRP) hypothalamiques et de la ghréline circulante comparé aux rats IR JI. Nous confirmons, l'augmentation des taux circulants de la gjhréline et du PYY chez le patient avec continuité jéjuno-colique. Il semble que l'absence de l'iléon (montage digestif jéjuno-colique) joue un rôle important dans la mise en place des signaux centraux et périphériques qui pourraient être impliqués dans l'hyperphagie. Nous avons mis en évidence l'acquisition de fonctions de l'intestin grêle par le colon résiduel, à savoir: augmentation de la fonction du transporteur SGLT-1 de glucose et de l'expression génique de l'AQP3, transporteur d'eau. Chez les rats IR, nous retrouvons du L-lactate, de l'acétate, du propionate mais pas de butyrate dans les fèces ce qui suggère la présence d'un microbiote dysbiotique. Enfm, le transfert du microbiote d'un patient SGC à risque de développer une encéphalopathie D-lactique chez le rat axénique, nous a permis de montrer que, bien que l'activité fermentaire intestinale soit modifiée, le microbiote transféré conserve des caractéristiques du microbiote du patient SGC à savoir une richesse en Lactobacillus et une absence en C. Leptum. Chez ces rats « humanisés », les taux circulants de GLP-1 et de ghréline et l'expression de SGLT-1 et AQP3 sont augmentés. Enfin, nous n'avons pas retrouvé la modification de neuropeptides hypothalamiques contrôlant la prise alimentaire chez ces animaux. Ces résultats indiquent que le microbiote intestinal du patient avec SGC est impliqué dans l'adaptation morpho-fonctionnelle de l'épithélium colique mais qu'il n'est pas suffisant pour établir le lien avec les neuropeptides hypothalamiques. L'ensemble de ces résultats permettent une meilleure compréhension des mécanismes de l'adaptation intestinale post-résection. Ils suggèrent fortement que le microbiote et le raccourcissement anatomique de l'intestin sont des acteurs importants de l'adaptation<br>The short bowel syndrome (SBS), results from a large resection of the small bowel, is the main cause of intestinal failure, which treatment is parenteral nutrition (PN). In the presence of colon in the continuity of the small intestine, an adaptation is iappeared and allows to reduce or to wean the patient from the NP. This adaptation is characterized by morphological and functional changes of the residual intestinal epithelium, by the appearance of hyperphagia in 70% of patients, and dysbiosis of the intestinal microbiota. The purpose of this work is to better understand the molecular, cellular and microbiological adaptation of the pathophysiology in the SGC. We have developed two models of intestinal resection in rats mimicking the SGC (IR) in digestive surgery with jejuno-colic anastomosis (JC) and jejuno-ileal anastomosis (JI). We show for the first time in the IR rat JC, an increased expression of orexigenic neuropeptides (NPY, AgRP) hypothalamic and circulating ghrelin compared to IR JI rats. We confirm the increase in circulating levels of ghrelin and PYY in patients with jejuno-colonic anastomosis. It seems that the absence of the ileum (jejuno-colic digestive assembly) plays an important role in the implementation of the central and peripheral signais that could be involved in hyperphagia. We have demonstrated the acquisition functions of the small intestine by the residual colon : increase in function SGLT-1 glucose transporter and gene expression of the AQP3, water carrier. In IR rats, we find L-lactate, acetate, propionate, butyrate, but not in the feces suggesting the presence of a dysbiotique microbiota. Finally, the transfer of the microbiota of a SBS patient at risk of developing a D-lactic encephalopathy in the germ free rat, allowed us to show that, although the intestinal fermentation activity is changed, the microbiota transferred retains the characteristics of the microbiota SGC patient namely a wealth of Lactobacillus and an absence C. Leptum. In such "humanized" rats, circulating levels of GLP-1 and ghrelin and expression of SGLT-1 and AQP3 are increased. Finally, we did not find the change of hypothalamic neuropeptides that control food intake in these animals. These results indicate that the intestinal microbiota of the patient with SGC is involved in the morpho-functional adaptation of the colonic epithelium, but it is not sufficient to establish a link with the hypothalamic neuropeptides. Ail these results allow a better understanding of the mechanisms of post-resection intestinal adaptation. They strongly suggest that the microbiota and the anatomical shortening of the intestine are important actors of adaptation
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Lemmey, Andrew Bruce. "Effects of insulin-like growth factors (IGFS) on recovery from gut resection in rats : a thesis submitted to the University of Adelaide, South Australia for the degree of Doctor of Philosophy / by Andrew Bruce Lemmey." 1992. http://hdl.handle.net/2440/21638.

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xxiii, 222 leaves : ill., plates ; 30 cm.<br>Title page, contents and abstract only. The complete thesis in print form is available from the University Library.<br>Shows that IGF-I peptides are effective in diminishing post-surgical catabolism and enhancing adaptive gut hyperplasia in rats recovering from massive small bowel resection.<br>Thesis (Ph.D.)--University of Adelaide, Dept. of Animal Science, 1992
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"Secretin as a neuropeptide in the rat cerebellum." 2001. http://library.cuhk.edu.hk/record=b5890880.

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Zhang Jie.<br>Thesis (M.Phil.)--Chinese University of Hong Kong, 2001.<br>Includes bibliographical references (leaves 54-74).<br>Abstracts in English and Chinese.<br>ACKNOWLEDGEMENTS --- p.i<br>ABSTRACT --- p.ii<br>ABSTRACT (Chinese) --- p.iv<br>ABBREVIATION --- p.vi<br>Chapter CHAPTER 1 --- INTRODUCTION --- p.1<br>Chapter 1.1 --- Overview of the study --- p.1<br>Chapter 1.2 --- Secretin --- p.3<br>Chapter 1.2.1 --- Discovery<br>Chapter 1.2.2 --- Molecular biology<br>Chapter 1.2.3 --- Biosynthesis and localization<br>Chapter 1.2.4 --- Function<br>Chapter 1.3 --- Secretin receptor --- p.8<br>Chapter 1.3.1 --- Molecular biology<br>Chapter 1.3.2 --- Localization<br>Chapter 1.3.3 --- Signal transduction pathway<br>Chapter 1.4 --- Secretin and autism --- p.13<br>Chapter 1.5 --- AMPA receptor --- p.15<br>Chapter 1.5.1 --- Molecular biology<br>Chapter 1.5.2 --- Localization<br>Chapter 1.5.3 --- Pharmacological property<br>Chapter 1.5.4 --- Function<br>Chapter 1.6 --- Cerebellum --- p.20<br>Chapter 1.6.1 --- Structure of the cerebellar cortex<br>Chapter 1.6.2 --- Neurons of the cerebellar cortex<br>Chapter 1.6.2.1 --- Granule cells<br>Chapter 1.6.2.2 --- Purkinje cells<br>Chapter 1.6.2.3 --- Basket and stellate cells<br>Chapter 1.6.2.4 --- Golgi cells<br>Chapter 1.6.3 --- Intrinsic circuitry of the cerebellar cortex<br>Chapter CHAPTER 2 --- METHODS AND MATERIALS --- p.25<br>Chapter 2.1 --- Brain slice preparation and maintenance --- p.25<br>Chapter 2.2 --- Experimental set-up --- p.26<br>Chapter 2.2.1 --- Visualization of neurons<br>Chapter 2.2.2 --- Electrophysiological recordings<br>Chapter 2.2.3 --- Evoked stimulation<br>Chapter 2.2.4 --- Drug preparation and administration<br>Chapter 2.3 --- Data analysis --- p.29<br>Chapter 2.3.1 --- Construction of dose-response curve<br>Chapter 2.3.2 --- Analysis of synaptic currents<br>Chapter 2.3.3 --- Statistics<br>Chapter CHAPTER 3 --- RESULTS --- p.31<br>Chapter 3.1 --- Basic characteristics of IPSCs recorded from PCs --- p.31<br>Chapter 3.1.1 --- Spontaneous IPSCs<br>Chapter 3.1.2 --- Miniature IPSCs<br>Chapter 3.1.3 --- Evoked IPSCs<br>Chapter 3.1.4 --- Rundown of IPSCs<br>Chapter 3.2 --- Electrophysiological effects of secretin --- p.33<br>Chapter 3.2.1 --- Effects of secretin on evoked IPSCs and EPSCs<br>Chapter 3.2.2 --- Effects of secretin on spontaneous IPSCs<br>Chapter 3.2.3 --- Effects of secretin on miniature IPSCs<br>Chapter 3.3 --- Mechanisms of secretin as a neuropeptide --- p.37<br>Chapter 3.3.1 --- Non-involvement of a postsynaptic site of action<br>Chapter 3.3.2 --- Non-involvement of calcium influx<br>Chapter 3.3.3 --- Involvement of cAMP second messenger<br>Chapter 3.3.4 --- Involvement of presynaptic AMP A receptors<br>Chapter 3.3.4.1 --- Glutamate-mediated action of secretin<br>Chapter 3.3.4.2 --- Effects of AMPA on miniature IPSCs<br>Chapter 3.3.4.3 --- Pharmacological evidence<br>Chapter CHAPTER 4 --- DISCUSSION --- p.45<br>Chapter 4.1 --- Secretin as a novel neuropeptide --- p.45<br>Chapter 4.2 --- Mechanisms of secretin --- p.46<br>Chapter 4.3 --- Physiological role of secretin in the cerebellum --- p.52<br>Chapter 4.4 --- Secretin and autism --- p.52<br>REFERENCES --- p.54
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Books on the topic "Gastrointestinal hormones Physiology"

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Falk Symposium (77th 1994 Freiburg im Breisgau, Germany). Gastrointestinal tract and endocrine system: Proceedings of the 77th Falk Symposium (part I of the Gastroenterology Week, Freiburg, 1994), held in Freiburg-im-Breisgau, Germany, June 12-14, 1994. Dordrecht: Kluwer Academic Publishers, 1995.

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Rolf, Håkanson, Sundler Frank, Lunds universitet. Dept. of Pharmacology., and Lunds universitet. Dept. of Medical Cell Research., eds. The stomach as an endocrine organ: Proceedings of the 15th Eric K. Fernström Symposium, held in Lund (Sweden) on 21-23 May 1990. Amsterdam: Elsevier, 1991.

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Rawdon, B. B. Gut endocrine cells in birds: An overview, with particular reference to the chemistry of gut peptides and the distribution, ontogeny, embryonic origin and differentiation of the endocrine cells. Jena, Germany: Urban & Fischer, 1999.

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Watson, Sue. Gastrin receptors in gastrointestinal tumors. Austin, Tex: R.G. Landes, 1993.

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Bersimbaev, Rakhmetkaji I. Cellular mechanisms in the regulation of gastric secretory cells. Landsberg: Ecomed, 1993.

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Reinecke, Manfred. Neurotensin: Immunohistochemical localization in central and peripheral nervous system and in endocrine cells and its functional role as neurotransmitter and endocrine hormone. Stuttgart: G. Fischer Verlag, 1985.

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H, Walsh John, and Dockray G. J, eds. Gut peptides: Biochemistry and physiology. New York: Raven Press, 1994.

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(Editor), John H. Walsh, and Graham J. Dockray (Editor), eds. Gut Peptides: Biochemistry and Physiology (Comprehensive Endocrinology, Revised Series). Raven Pr, 1994.

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H, Greeley George, ed. Gastrointestinal endocrinology. Totowa, N.J: Humana Press, 1999.

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E, Daniel E., ed. Neuropeptide function in the gastrointestinal tract. Boca Raton, Fla: CRC Press, 1991.

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Book chapters on the topic "Gastrointestinal hormones Physiology"

1

Welcome, Menizibeya Osain. "Gastrointestinal Hormones." In Gastrointestinal Physiology, 455–526. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91056-7_8.

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Valle, John Del. "Gastrointestinal hormones in the regulation of gut function in health and disease." In Gastrointestinal Anatomy and Physiology, 15–32. Oxford: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118833001.ch2.

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Pramanik, Debasis. "Gastrointestinal hormones." In Principles of Physiology, 360. Jaypee Brothers Medical Publishers (P) Ltd., 2015. http://dx.doi.org/10.5005/jp/books/12674_45.

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Sembulingam, K., and Prema Sembulingam. "Gastrointestinal Hormones." In Essentials of Medical Physiology, 281. Jaypee Brothers Medical Publishers (P) Ltd., 2012. http://dx.doi.org/10.5005/jp/books/11696_122.

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Sembulingam, K., and Prema Sembulingam. "Gastrointestinal Hormones." In Essentials of Medical Physiology, 268. Jaypee Brothers Medical Publishers (P) Ltd., 2010. http://dx.doi.org/10.5005/jp/books/11093_44.

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Sembulingam, K., and Prema Sembulingam. "Gastrointestinal Hormones." In Essentials of Medical Physiology, 254. Jaypee Brothers Medical Publishers (P) Ltd., 2006. http://dx.doi.org/10.5005/jp/books/10283_44.

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Gribble, Fiona M., Frank Reimann, and Geoffrey P. Roberts. "Gastrointestinal Hormones ☆." In Physiology of the Gastrointestinal Tract, 31–70. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-809954-4.00002-5.

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Pal, Gopal, Pravati Pal, and Nivedita Nanda. "Gastrointestinal Hormones." In Comprehensive Textbook of Medical Physiology (Volume 1), 335. Jaypee Brothers Medical Publishers (P) Ltd., 2017. http://dx.doi.org/10.5005/jp/books/12960_38.

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"Gastrointestinal Hormones: II (Gastrins)." In Metabolic and Endocrine Physiology, 108–9. Teton NewMedia, 2012. http://dx.doi.org/10.1201/b16175-52.

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NM, Muthayya. "Chapter-05 Gastrointestinal Hormones." In Human Physiology (4th ed), 168–71. NM Muthayya, 2009. http://dx.doi.org/10.5005/jp/books/10366_20.

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