Journal articles: '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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Kunnimalaiyaan, Muthusamy, Kelly Traeger, and Herbert Chen. "Conservation of the Notch1 signaling pathway in gastrointestinal carcinoid cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 4 (October 2005): G636—G642. http://dx.doi.org/10.1152/ajpgi.00146.2005.

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Gastrointestinal (GI) carcinoid cells secrete multiple neuroendocrine (NE) markers and hormones including 5-hydroxytryptamine and chromogranin A. We were interested in determining whether activation of the Notch1 signal transduction pathway in carcinoid cells could modulate production of NE markers and hormones. Human pancreatic carcinoid cells (BON cells) were stably transduced with an estrogen-inducible Notch1 construct, creating BON-NIER cells. In the present study, we found that Notch1 is not detectable in human GI carcinoid tumor cells. The induction of Notch1 in human BON carcinoid cells led to high levels of functional Notch1, as measured by CBF-1 binding studies, resulting in activation of the Notch1 pathway. Similar to its developmental role in the GI tract, Notch1 pathway activation led to an increase in hairy enhancer of split 1 (HES-1) protein and a concomitant silencing of human Notch1/HES-1/achaete-scute homolog 1. Furthermore, Notch1 activation led to a significant reduction in NE markers. Most interestingly, activation of the Notch1 pathway caused a significant reduction in 5-hydroxytryptamine, an important bioactive hormone in carcinoid syndrome. In addition, persistent activation of the Notch1 pathway in BON cells led to a notable reduction in cellular proliferation. These results demonstrate that the Notch1 pathway, which plays a critical role in the differentiation of enteroendocrine cells, is highly conserved in the gut. Therefore, manipulation of the Notch1 signaling pathway may be useful for expanding the targets for therapeutic and palliative treatment of patients with carcinoid tumors.

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Walton, Kristen L. W. "Teaching the role of secretin in the regulation of gastric acid secretion using a classic paper by Johnson and Grossman." Advances in Physiology Education 33, no. 3 (September 2009): 165–68. http://dx.doi.org/10.1152/advan.00023.2009.

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The regulation of gastric acid secretion has been the subject of investigation for over a century. Inhibition of gastrin-induced acid secretion by the intestine-derived hormone secretin provides a classic physiological example of negative feedback in the gastrointestinal tract. A classic paper by Leonard R. Johnson and Morton I. Grossman clearly shows the ability of secretin to negatively regulate gastric acid secretion, providing students with an example of this feedback loop. In addition, this article demonstrates the step forward in gastrointestinal endocrinology that occurred when pure preparations of secretin and other gastrointestinal hormones first became available. The comparison of the effects of exogenous, purified secretin to the physiological stimulus of acid in the duodenum is an important example of how newly available reagents allow scientists such as Johnson and Grossman to clarify the mechanisms behind previously established processes. One or more figures from this classic paper can be used to give students insight into the role of secretin in the regulation of the function of the gastrointestinal tract and will also give students a clear example of how the careful experimentation and clear interest in gastrointestinal physiology led Johnson and Grossman to advance the field.

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Seidel, E. R. "Hormonal regulation of postprandial induction of gastrointestinal ornithine decarboxylase activity." American Journal of Physiology-Gastrointestinal and Liver Physiology 251, no. 4 (October 1, 1986): G460—G466. http://dx.doi.org/10.1152/ajpgi.1986.251.4.g460.

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The growth of gastrointestinal mucosa can be related to ingestion and digestion of diet, with fasting producing mucosal hypoplasia and hyperphagia producing mucosal hyperplasia. Experiments were designed to determine whether induction of polyamine metabolism following ingestion of a meal was related to mucosal growth. Activity of the enzyme ornithine decarboxylase (ODC) in both jejunum and ileum but not in duodenum was dependent on the presence of food in the gut; ODC activity was more than 200-fold greater in mucosa of fed rats than in fasted rats. Inhibition of ODC with difluoromethylornithine lead to mucosal atrophy in ileum but not in duodenum. Refeeding of fasted rats resulted in significant induction of ODC in duodenal, ileal, and colonic, but not fundic, mucosa. In addition, two hormones, epidermal growth factor and glucagon, were effective inducers of ileal ODC activity. Direct evidence for hormonal involvement in the postprandial rise in mucosal ODC activity was provided by experiments in rats that had undergone ileal bypass surgery. After refeeding of fasted rats mucosal ODC activity was induced in both ileum left in continuity and in the bypassed segment. Refeeding of elemental diets demonstrated that ingestion of carbohydrate alone was sufficient for maximal enzyme induction. Mixed amino acids or glyceryl trioleate were no more effective inducers than nonnutritive solutions of cellulose or saccharin. These data demonstrate that hormones which are released during ingestion and digestion of a meal are the stimuli for induction of mucosal polyamine metabolism, suggesting that food-induced mucosal growth is hormonally mediated.

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Murphy, M. S., A. L. Brunetto, A. D. J. Pearson, M. A. Ghatei, R. Nelson, E. J. Eastham, S. R. Bloom, and A. Aynsley Green. "Gut hormones and gastrointestinal motility in children with cystic fibrosis." Digestive Diseases and Sciences 37, no. 2 (February 1992): 187–92. http://dx.doi.org/10.1007/bf01308170.

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Buchan, Alison M. J. "III. Endocrine cell recognition of luminal nutrients." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 6 (December 1, 1999): G1103—G1107. http://dx.doi.org/10.1152/ajpgi.1999.277.6.g1103.

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The profile of hormone secretion from the gastrointestinal tract on food ingestion depends to a great extent on the composition of the meal. High levels of protein result in a quantitatively and qualitatively different response compared with a meal rich in fats. The outstanding question is whether this differential response is driven by the ability of gastroenteric endocrine cells to directly sense the contents of the lumen via apical microvilli. Alternative effectors would include activation of the intrinsic and extrinsic innervation or other epithelial cell populations. The data available indicate that the role of the gastrointestinal innervation is relatively limited and is probably a major factor only in the postprandial responses of hormones released from endocrine cells in the distal small intestine. However, whether nutrients directly stimulate gastroenteric endocrine cells or another epithelial cell type has yet to be established.

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Steinert, R. E., C. Feinle-Bisset, N. Geary, and C. Beglinger. "DIGESTIVE PHYSIOLOGY OF THE PIG SYMPOSIUM: Secretion of gastrointestinal hormones and eating control1." Journal of Animal Science 91, no. 5 (May 1, 2013): 1963–73. http://dx.doi.org/10.2527/jas.2012-6022.

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Busnelli, Marco, Stefano Manzini, and Giulia Chiesa. "The Gut Microbiota Affects Host Pathophysiology as an Endocrine Organ: A Focus on Cardiovascular Disease." Nutrients 12, no. 1 (December 27, 2019): 79. http://dx.doi.org/10.3390/nu12010079.

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It is widely recognized that the microorganisms inhabiting our gastrointestinal tract—the gut microbiota—deeply affect the pathophysiology of the host. Gut microbiota composition is mostly modulated by diet, and gut microorganisms communicate with the different organs and tissues of the human host by synthesizing hormones and regulating their release. Herein, we will provide an updated review on the most important classes of gut microbiota-derived hormones and their sensing by host receptors, critically discussing their impact on host physiology. Additionally, the debated interplay between microbial hormones and the development of cardiovascular disease will be thoroughly analysed and discussed.

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Dickinson, CJ, C. Seva, and T. Yamada. "Gastrin Processing: From Biochemical Obscurity to Unique Physiological Actions." Physiology 12, no. 1 (February 1, 1997): 9–15. http://dx.doi.org/10.1152/physiologyonline.1997.12.1.9.

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Posttranslational processing is essential for the biological activation of many peptide hormones. Only fully processed and amidated gastrin, a peptide secreted by the stomach, stimulates acid secretion. However, both amidated gastrin and its glycine-extended precursor stimulate cellular proliferation through selective receptors, suggesting that posttranslational processing is critical to gastrointestinal physiology.

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Petersen, OH. "Generation of cytosolic calcium signals by gastrointestinal hormones." Regulatory Peptides 40, no. 2 (July 1992): 226. http://dx.doi.org/10.1016/0167-0115(92)90370-a.

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Raka, Fitore, Sarah Farr, Jacalyn Kelly, Alexandra Stoianov, and Khosrow Adeli. "Metabolic control via nutrient-sensing mechanisms: role of taste receptors and the gut-brain neuroendocrine axis." American Journal of Physiology-Endocrinology and Metabolism 317, no. 4 (October 1, 2019): E559—E572. http://dx.doi.org/10.1152/ajpendo.00036.2019.

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Nutrient sensing plays an important role in ensuring that appropriate digestive or hormonal responses are elicited following the ingestion of fuel substrates. Mechanisms of nutrient sensing in the oral cavity have been fairly well characterized and involve lingual taste receptors. These include heterodimers of G protein-coupled receptors (GPCRs) of the taste receptor type 1 (T1R) family for sensing sweet (T1R2-T1R3) and umami (T1R1-T1R3) stimuli, the T2R family for sensing bitter stimuli, and ion channels for conferring sour and salty tastes. In recent years, several studies have revealed the existence of additional nutrient-sensing mechanisms along the gastrointestinal tract. Glucose sensing is achieved by the T1R2-T1R3 heterodimer on enteroendocrine cells, which plays a role in triggering the secretion of incretin hormones for improved glycemic and lipemic control. Protein hydrolysates are detected by Ca2+-sensing receptor, the T1R1-T1R3 heterodimer, and G protein-coupled receptor 92/93 (GPR92/93), which leads to the release of the gut-derived satiety factor cholecystokinin. Furthermore, several GPCRs have been implicated in fatty acid sensing: GPR40 and GPR120 respond to medium- and long-chain fatty acids, GPR41 and GPR43 to short-chain fatty acids, and GPR119 to endogenous lipid derivatives. Aside from the recognition of fuel substrates, both the oral cavity and the gastrointestinal tract also possess T2R-mediated mechanisms of recognizing nonnutrients such as environmental contaminants, bacterial toxins, and secondary plant metabolites that evoke a bitter taste. These gastrointestinal sensing mechanisms result in the transmission of neuronal signals to the brain through the release of gastrointestinal hormones that act on vagal and enteric afferents to modulate the physiological response to nutrients, particularly satiety and energy homeostasis. Modulating these orally accessible nutrient-sensing pathways using particular foods, dietary supplements, or pharmaceutical compounds may have therapeutic potential for treating obesity and metabolic diseases.

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Thomson, A. B. R., and M. Keelan. "The development of the small intestine." Canadian Journal of Physiology and Pharmacology 64, no. 1 (January 1, 1986): 13–29. http://dx.doi.org/10.1139/y86-003.

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The remarkable degree of coordination between the development of various aspects of gastrointestinal function suggests that the process may be triggered by a single or a few central mechanisms, such as weaning and (or) hormones. Precocious development of enzyme and transport function can be induced by exogenous thyroxine and corticosteroids, while thyroidectomy and adrenalectomy abolish the normal pattern of postnatal development. These hormones may have a primary or a permissive role. Activation of the dormant hormonal mechanism could be controlled by a genetically coded biologic clock, such as chronologic age, or by a biological signal such as body size and oral intake. Generally speaking, shortly after birth, there are increases in the intestinal mucosal surface area, brush border membrane enzymes, and carrier-mediated transport. These adaptive changes occur as a result of the genetic endowment of the animal, but may be modified by environmental factors, particularly nutrient intake.

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Malfertheiner, P., M. G. Sarr, M. P. Spencer, and E. P. DiMagno. "Effect of duodenectomy on interdigestive pancreatic secretion, gastrointestinal motility, and hormones in dogs." American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no. 3 (September 1, 1989): G415—G422. http://dx.doi.org/10.1152/ajpgi.1989.257.3.g415.

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We tested the hypothesis that the duodenum is necessary to coordinate interdigestive pancreatic trypsin secretion with gastrointestinal motility and determined whether duodenectomy altered interdigestive cycles of plasma motilin and pancreatic polypeptide and their relationship to trypsin secretion and motility. Consequently, in normal and duodenectomized dogs, we measured trypsin secretion, gastrointestinal motility, and plasma concentrations of motilin and pancreatic polypeptide during the interdigestive period. After duodenectomy, peaks of trypsin secretion continued to cycle at normal intervals (102 +/- 15 min), but the amounts of trypsin were reduced during peaks of secretion (P = 0.02) and throughout the entire cycle (P = 0.02). Trypsin secretory cycles after duodenectomy, however, were not coordinated with cycles of interdigestive motility, and the plasma concentrations of motilin (P = 0.02) and pancreatic polypeptide (P = 0.05) were reduced and had no cyclic pattern. In addition, we confirmed that duodenectomy alters canine interdigestive antral motility, interrupts coordination between antral and intestinal motility, and shortens the period of jejunal migrating motor complexes. We conclude that duodenectomy disrupts the relationship between the cycles of interdigestive gastrointestinal motility and trypsin secretion and reduces the amount of interdigestive trypsin secretion. These effects of duodenectomy may be due to interruption of the duodenopancreatic neural connections or the hormonal abnormalities we have described. The loss of the cyclic pattern of plasma pancreatic polypeptide after duodenectomy suggests that the duodenum controls the release of pancreatic polypeptide by either a neural or hormonal mechanism.

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Kanno, Noriatsu, Gene LeSage, Shannon Glaser, and Gianfranco Alpini. "Regulation of cholangiocyte bicarbonate secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 3 (September 1, 2001): G612—G625. http://dx.doi.org/10.1152/ajpgi.2001.281.3.g612.

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The objective of this review article is to discuss the role of secretin and its receptor in the regulation of the secretory activity of intrahepatic bile duct epithelial cells (i.e., cholangiocytes). After a brief overview of cholangiocyte functions, we provide an historical background for the role of secretin and its receptor in the regulation of ductal secretion. We review the newly developed experimental in vivo and in vitro tools, which lead to understanding of the mechanisms of secretin regulation of cholangiocyte functions. After a description of the intracellular mechanisms by which secretin stimulates ductal secretion, we discuss the heterogeneous responses of different-sized intrahepatic bile ducts to gastrointestinal hormones. Furthermore, we outline the role of a number of cooperative factors (e.g., nerves, alkaline phosphatase, gastrointestinal hormones, neuropeptides, and bile acids) in the regulation of secretin-stimulated ductal secretion. Finally, we discuss other factors that may also play an important role in the regulation of secretin-stimulated ductal secretion.

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Gruzdeva, O. V., D. A. Borodkina, E. V. Belik, O. E. Akbasheva, E. I. Palicheva, and O. L. Barbarash. "Ghrelin Physiology and Pathophysiology: Focus on the Cardiovascular System." Kardiologiia 59, no. 3 (April 13, 2019): 60–67. http://dx.doi.org/10.18087/cardio.2019.3.10220.

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Ghrelin is a multifunctional peptide hormone, mainly synthesized by P / D1 cells of the stomach fundus mucosa. Its basic effect, which is realized via GHS-R1 α receptor in the arcuate and the ventromedial nucleuses of hypothalamus, is stimulation of the synthesis of pituitary hormones. Ghrelin is involved in control of appetite and energy balance, regulation of carbohydrate and lipid metabolism, cell proliferation and apoptosis, as well as modulation of functioning of gastrointestinal, cardiovascular, pulmonary and immune systems. It was found that cardiomyocytes are able to synthesize ghrelin. High concentrations of GHS-R1α in the heart and major blood vessels evidence for its possible participation in functioning of cardiovascular system. Ghrelin inhibits apoptosis of cardiomyocytes and endothelial cells, and improves the functioning of the left ventricle (LV) after injury of ischemia-reperfusion mechanism. In rats with heart failure (HF) ghrelin improves LV function and attenuates development of cardiac cachexia. In addition, ghrelin exerts vasodilatory effects in humans, improves cardiac function and reduces peripheral vascular resistance in patients with chronic HF. The review contains of the predictive value of ghrelin in the development and prevention of cardiovascular disease.

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Albrechtsen, Nicolai J. Wewer, and Jens F. Rehfeld. "On premises and principles for measurement of gastrointestinal peptide hormones." Peptides 141 (July 2021): 170545. http://dx.doi.org/10.1016/j.peptides.2021.170545.

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Riediger, Thomas, Nicole Eisele, Caroline Scheel, and Thomas A. Lutz. "Effects of glucagon-like peptide 1 and oxyntomodulin on neuronal activity of ghrelin-sensitive neurons in the hypothalamic arcuate nucleus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 4 (April 2010): R1061—R1067. http://dx.doi.org/10.1152/ajpregu.00438.2009.

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Glucagon-like peptide 1 (GLP-1) and oxyntomodulin (OXM) are structurally related gastrointestinal hormones that are secreted in response to food intake. They reduce food intake and body weight and exert partly overlapping actions on glucose homeostasis and gastrointestinal function. The hypothalamic arcuate (ARC) nucleus is among the central structures expressing a high density of GLP-1 receptors (GLP-1R), which are known to be activated by both peptides. It was the aim of our electrophysiological studies to characterize the effects of GLP-1 and OXM on functionally defined ghrelin-sensitive ARC neurons. GLP-1 and OXM (10−7 M) exerted excitatory effects in about two-thirds of ghrelin-inhibited neurons and in approximately one-third of ghrelin-excited cells. In addition, a minor fraction of the ghrelin-excited cells was inhibited by both peptides. There was a high degree of cosensitivity to GLP-1 and OXM, and the effects of both hormones were blocked by the GLP-1R antagonist exendin(9–39). The GLP-1R-mediated excitations and inhibitions persisted under synaptic blockade, indicating a direct postsynaptic mode of action. Our results demonstrate that GLP-1 and OXM directly and similarly alter neuronal activity in the ARC, probably via a common GLP-1R-mediated mechanism. Ghrelin-antagonistic effects on neuronal activity, which might be implicated in ghrelin-antagonistic in vivo actions, resulting from GLP-1R stimulation (e.g., GLP-1R dependent supression of food intake), predominated in ghrelin-inhibited ARC neurons. However, a subset of ghrelin-excited ARC neurons showed responses to OXM or GLP-1, suggesting the existence of a common mode of action for these hormones; the functional relevance of this effect remains to be elucidated.

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Xie, Cong, Weikun Huang, Richard L. Young, Karen L. Jones, Michael Horowitz, Christopher K. Rayner, and Tongzhi Wu. "Role of Bile Acids in the Regulation of Food Intake, and Their Dysregulation in Metabolic Disease." Nutrients 13, no. 4 (March 28, 2021): 1104. http://dx.doi.org/10.3390/nu13041104.

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Bile acids are cholesterol-derived metabolites with a well-established role in the digestion and absorption of dietary fat. More recently, the discovery of bile acids as natural ligands for the nuclear farnesoid X receptor (FXR) and membrane Takeda G-protein-coupled receptor 5 (TGR5), and the recognition of the effects of FXR and TGR5 signaling have led to a paradigm shift in knowledge regarding bile acid physiology and metabolic health. Bile acids are now recognized as signaling molecules that orchestrate blood glucose, lipid and energy metabolism. Changes in FXR and/or TGR5 signaling modulates the secretion of gastrointestinal hormones including glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), hepatic gluconeogenesis, glycogen synthesis, energy expenditure, and the composition of the gut microbiome. These effects may contribute to the metabolic benefits of bile acid sequestrants, metformin, and bariatric surgery. This review focuses on the role of bile acids in energy intake and body weight, particularly their effects on gastrointestinal hormone secretion, the changes in obesity and T2D, and their potential relevance to the management of metabolic disorders.

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Hornnes, Peter J., and Claus Kühl. "Gastrointestinal hormones and cortisol in normal pregnant women and women with gestational diabetes." Acta Endocrinologica 113, no. 3_Suppl (August 1986): S24—S26. http://dx.doi.org/10.1530/acta.0.111s0024.

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Abstract. In pregnancy the secretion of a number of gastro-enteropancreatic hormones is considerably altered. These changes might be involved in the gestational modification of gastrointestinal physiology. The enteral stimulation of insulin secretion (the incretin effect) is diminished in pregnancy – both when determined indirectly and when the gastric inhibitory polypeptide (GIP) response to glucose ingestion is considered. Whether this is important for the deterioration of glucose tolerance in pregnancy is uncertain. In gestational diabetics similar findings as in normal pregnant women were obtained except that the GIP response to glucose ingestion was smaller and the GIP response to lipid ingestion greater than in normal women. It is, however, unlikely that these differences are responsible for the development of gestational diabetes. Significant positive correlations were found between the increase of plasma cortisol levels during normal pregnancy and the concomitant decrease in glucose tolerance indicating that the increased cortisol levels might be involved in the development of the insulin resistance found in normal pregnancy.

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Graffner, H., S. R. Bloom, L. O. Farnebo, and J. J�rhult. "Effects of physiological increases of plasma noradrenaline on gastric acid secretion and gastrointestinal hormones." Digestive Diseases and Sciences 32, no. 7 (July 1987): 715–19. http://dx.doi.org/10.1007/bf01296137.

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McCauley, Heather A. "Enteroendocrine Regulation of Nutrient Absorption." Journal of Nutrition 150, no. 1 (August 27, 2019): 10–21. http://dx.doi.org/10.1093/jn/nxz191.

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ABSTRACT Enteroendocrine cells (EECs) in the intestine regulate many aspects of whole-body physiology and metabolism. EECs sense luminal and circulating nutrients and respond by secreting hormones that act on multiple organs and organ systems, such as the brain, gallbladder, and pancreas, to control satiety, digestion, and glucose homeostasis. In addition, EECs act locally, on enteric neurons, endothelial cells, and the gastrointestinal epithelium, to facilitate digestion and absorption of nutrients. Many recent reports raise the possibility that EECs and the enteric nervous system may coordinate to regulate gastrointestinal functions. Loss of all EECs results in chronic malabsorptive diarrhea, placing EECs in a central role regulating nutrient absorption in the gut. Because there is increasing evidence that EECs can directly modulate the efficiency of nutrient absorption, it is possible that EECs are master regulators of a feed-forward loop connecting appetite, digestion, metabolism, and abnormally augmented nutrient absorption that perpetuates metabolic disease. This review focuses on the roles that specific EEC hormones play on glucose, peptide, and lipid absorption within the intestine.

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Resch-Sedlmeier, G., and D. Sedlmeier. "Release of digestive enzymes from the crustacean hepatopancreas: effect of vertebrate gastrointestinal hormones." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 123, no. 2 (June 1999): 187–92. http://dx.doi.org/10.1016/s0305-0491(99)00056-5.

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Michell, A. R., E. S. Debnam, and R. J. Unwin. "Regulation of Renal Function by the Gastrointestinal Tract: Potential Role of Gut-Derived Peptides and Hormones." Annual Review of Physiology 70, no. 1 (March 2008): 379–403. http://dx.doi.org/10.1146/annurev.physiol.69.040705.141330.

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Dong, Tien S., John P. Vu, Suwan Oh, Daniel Sanford, Joseph R. Pisegna, and Patrizia Germano. "Intraperitoneal Treatment of Kisspeptin Suppresses Appetite and Energy Expenditure and Alters Gastrointestinal Hormones in Mice." Digestive Diseases and Sciences 65, no. 8 (November 15, 2019): 2254–63. http://dx.doi.org/10.1007/s10620-019-05950-7.

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Tordoff, M. G., S. J. Fluharty, and J. Schulkin. "Physiological consequences of NaCl ingestion by Na(+)-depleted rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 2 (August 1, 1991): R289—R295. http://dx.doi.org/10.1152/ajpregu.1991.261.2.r289.

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We investigated the temporal relationships between NaCl intake, gastrointestinal Na+ content, and plasma concentrations of Na+, aldosterone, and plasma renin activity (angiotensin). Rats depleted of approximately 2.2 mmol Na+ by combined dietary Na+ restriction and furosemide injection (10 mg sc) drank a preload of 1, 2, or 3 mmol 0.5 M NaCl. Intake of a test 0.5 M NaCl solution given 15, 30, 60, or 120 min later was reduced by approximately 50% of the preload content, irrespective of the interval between preload and test. At 15 min after starting to drink, 61-71% of ingested Na+ remained in the stomach, 15-18% in the small intestine, approximately 5% was calculated to be in extracellular fluid, and less than 1% was excreted. Rates of gastric and gastrointestinal clearance of Na+ were related to the quantity of NaCl ingested. Whereas gastric emptying was initially very rapid (30-61 mumol/min) and decreased with time, gastrointestinal clearance was constant (16-39 mumol/min). Drinking 3 mmol NaCl reliably reduced plasma aldosterone concentrations within 15 min and renin activity within 30 min. Drinking 1 or 2 mmol NaCl reliably reduced levels of these hormones within 30-60 min. The results describe for the first time the distribution of Na+ after Na(+)-depleted rats drink NaCl. They suggest that the rat determines the quantity of Na+ it requires within the first 15 min of ingestion and thus does not depend on signals generated by the prolonged influence of Na+ in the gastrointestinal tract or the fall in plasma concentrations of aldosterone and angiotensin.

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Mackie, Alan R., Balazs H. Bajka, Neil M. Rigby, Peter J. Wilde, Fatima Alves-Pereira, Ellen F. Mosleth, Anne Rieder, Bente Kirkhus, and Louise J. Salt. "Oatmeal particle size alters glycemic index but not as a function of gastric emptying rate." American Journal of Physiology-Gastrointestinal and Liver Physiology 313, no. 3 (September 1, 2017): G239—G246. http://dx.doi.org/10.1152/ajpgi.00005.2017.

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The aim of this study was to determine the extent to which oat particle size in a porridge could alter glucose absorption, gastric emptying, gastrointestinal hormone response, and subjective feelings of appetite and satiety. Porridge was prepared from either oat flakes or oat flour with the same protein, fat, carbohydrate, and mass. These were fed to eight volunteers on separate days in a crossover study, and subjective appetite ratings, gastric contents, and plasma glucose, insulin, and gastrointestinal hormones were determined over a period of 3 h. The flake porridge gave a lower glucose response than the flour porridge, and there were apparent differences in gastric emptying in both the early and late postprandial phases. The appetite ratings showed similar differences between early- and late-phase behavior. The structure of the oat flakes remained sufficiently intact to delay their gastric emptying, leading to a lower glycemic response, even though initial gastric emptying rates were similar for the flake and flour porridge. This highlights the need to take food structure into account when considering relatively simple physiological measures and offering nutritional guidance.NEW & NOTEWORTHY The impact of food structure on glycemic response even in simple foods such as porridge is dependent on both timing of gastric emptying and the composition of what is emptied as well as duodenal starch digestion. Thus structure should be accounted for when considering relatively simple physiological measures and offering nutritional guidance.

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Thaler, Joshua P., and David E. Cummings. "Hormonal and Metabolic Mechanisms of Diabetes Remission after Gastrointestinal Surgery." Endocrinology 150, no. 6 (April 16, 2009): 2518–25. http://dx.doi.org/10.1210/en.2009-0367.

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Bariatric surgery is the most effective available treatment for obesity. The most frequently performed operation, Roux-en-Y gastric bypass (RYGB), causes profound weight loss and ameliorates obesity-related comorbid conditions, especially type 2 diabetes mellitus (T2DM). Approximately 84% of diabetic patients experience complete remission of T2DM after undergoing RYGB, often before significant weight reduction. The rapid time course and disproportional degree of T2DM improvement after RYGB compared with equivalent weight loss from other interventions suggest surgery-specific, weight-independent effects on glucose homeostasis. Potential mechanisms underlying the direct antidiabetic impact of RYGB include enhanced nutrient stimulation of lower intestinal hormones (e.g. glucagon-like peptide-1), altered physiology from excluding ingested nutrients from the upper intestine, compromised ghrelin secretion, modulations of intestinal nutrient sensing and regulation of insulin sensitivity, and other changes yet to be fully characterized. Research aimed at determining the relative importance of these effects and identifying additional mechanisms promises not only to improve surgical design but also to identify novel targets for diabetes medications.

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Stanley, Sarah, Katie Wynne, Barbara McGowan, and Stephen Bloom. "Hormonal Regulation of Food Intake." Physiological Reviews 85, no. 4 (October 2005): 1131–58. http://dx.doi.org/10.1152/physrev.00015.2004.

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Our knowledge of the physiological systems controlling energy homeostasis has increased dramatically over the last decade. The roles of peripheral signals from adipose tissue, pancreas, and the gastrointestinal tract reflecting short- and long-term nutritional status are now being described. Such signals influence central circuits in the hypothalamus, brain stem, and limbic system to modulate neuropeptide release and hence food intake and energy expenditure. This review discusses the peripheral hormones and central neuronal pathways that contribute to control of appetite.

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Chandwe, Kanta, and Paul Kelly. "Colostrum Therapy for Human Gastrointestinal Health and Disease." Nutrients 13, no. 6 (June 7, 2021): 1956. http://dx.doi.org/10.3390/nu13061956.

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There is increasing awareness that a broad range of gastrointestinal diseases, and some systemic diseases, are characterized by failure of the mucosal barrier. Bovine colostrum is a complex biological fluid replete with growth factors, nutrients, hormones, and paracrine factors which have a range of properties likely to contribute to mucosal healing in a wide range of infective, inflammatory, and injury conditions. In this review, we describe the anatomy and physiology of the intestinal barrier and how it may fail. We survey selected diseases in which disordered barrier function contributes to disease pathogenesis or progression, and review the evidence for or against efficacy of bovine colostrum in management. These disorders include enteropathy due to non-steroidal anti-inflammatory drugs (NSAIDs), inflammatory bowel disease (IBD), necrotizing enterocolitis, infectious diarrhea, intestinal failure, and damage due to cancer therapy. In animal models, bovine colostrum benefits NSAID enteropathy, IBD, and intestinal failure. In human trials, there is substantial evidence of efficacy of bovine colostrum in inflammatory bowel disease and in infectious diarrhea. Given the robust scientific rationale for using bovine colostrum as a promoter of mucosal healing, further work is needed to define its role in therapy.

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Yamatani, Keiichi, Norihiro Sato, Kenji Takahashi, Masao Hara, and Hideo Sasaki. "Effect of gastrointestinal hormones on choleresis from the isolated perfused rat liver." Regulatory Peptides 10, no. 2-3 (March 1985): 237–42. http://dx.doi.org/10.1016/0167-0115(85)90018-7.

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Littlejohn, Erica L., Liliana Espinoza, Monica M. Lopez, Bret N. Smith, and Carie R. Boychuk. "GABAA receptor currents in the dorsal motor nucleus of the vagus in females: influence of ovarian cycle and 5α-reductase inhibition." Journal of Neurophysiology 122, no. 5 (November 1, 2019): 2130–41. http://dx.doi.org/10.1152/jn.00039.2019.

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The dorsal motor nucleus of the vagus (DMV) contains the preganglionic motor neurons important in the regulation of glucose homeostasis and gastrointestinal function. Despite the role of sex in the regulation of these processes, few studies examine the role of sex and/or ovarian cycle in the regulation of synaptic neurotransmission to the DMV. Since GABAergic neurotransmission is critical to normal DMV function, the present study used in vitro whole cell patch-clamping to investigate whether sex differences exist in GABAergic neurotransmission to DMV neurons. It additionally investigated whether the ovarian cycle plays a role in those sex differences. The frequency of phasic GABAA receptor-mediated inhibitory postsynaptic currents in DMV neurons from females was lower compared with males, and this effect was TTX sensitive and abolished by ovariectomy (OVX). Amplitudes of GABAergic currents (both phasic and tonic) were not different. However, females demonstrated significantly more variability in the amplitude of both phasic and tonic GABAA receptor currents. This difference was eliminated by OVX in females, suggesting that these differences were related to reproductive hormone levels. This was confirmed for GABAergic tonic currents by comparing females in two ovarian stages, estrus versus diestrus. Female mice in diestrus had larger tonic current amplitudes compared with those in estrus, and this increase was abolished after administration of a 5α-reductase inhibitor but not modulation of estrogen. Taken together, these findings demonstrate that DMV neurons undergo GABAA receptor activity plasticity as a function of sex and/or sex steroids. NEW & NOTEWORTHY Results show that GABAergic signaling in dorsal vagal motor neurons (DMV) demonstrates sex differences and fluctuates across the ovarian cycle in females. These findings are the first to demonstrate that female GABAA receptor activity in this brain region is modulated by 5α-reductase-dependent hormones. Since DMV activity is critical to both glucose and gastrointestinal homeostasis, these results suggest that sex hormones, including those synthesized by 5α-reductase, contribute to visceral, autonomic function related to these physiological processes.

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Brandler, Justin, Laurence J. Miller, Xiao Jing Wang, Duane Burton, Irene Busciglio, Kayla Arndt, William S. Harmsen, and Michael Camilleri. "Secretin effects on gastric functions, hormones and symptoms in functional dyspepsia and health: randomized crossover trial." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 4 (April 1, 2020): G635—G645. http://dx.doi.org/10.1152/ajpgi.00371.2019.

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Abnormal gastric accommodation (GA) and gastric emptying contribute to pathophysiology in functional dyspepsia (FD). Secretin is a key regulator of GA in animal studies. Our aim was to study the effects of secretin on gastric motility, satiation, postprandial symptoms, and key hormones. We performed two double-blind, randomized, saline-controlled crossover trials in 10 healthy volunteers and 10 patients with FD by Rome IV criteria. We used measured GA (by validated SPECT method) after a 111In radiolabeled Ensure 300-mL meal and quantified gastric emptying for 30 min by scintigraphy. Satiation was measured by volume to fullness (VTF) and maximum tolerated volume (MTV) on an Ensure nutrient drink test and postprandial symptoms 30 min post-MTV. Fasting and postprandial GLP-1, GIP, and HPP were measured. The ages and sex distribution of healthy controls and patients with FD were similar. Compared with placebo, secretin delayed gastric emptying at 30 min in both health [−11% (−16, −4), P = 0.004]; and FD [−8% (−9, 0), P = 0.03]. Satiation (VTF and MTV), GA, and plasma levels of GLP-1, GIP, and HPP did not differ between treatment arms in health or FD. On ANCOVA analysis (adjusting for age and sex), secretin did not consistently increase postprandial symptoms in health or FD. Secretin delayed gastric emptying in both health and FD without significantly altering GA, VTF, or MTV or selected hormones. Thus, secretin receptor activation may provide a novel therapeutic mechanism for patients with FD and rapid gastric emptying. NEW & NOTEWORTHY The naturally occurring hormone secretin retards gastric emptying of solids without deleteriously affecting gastric accommodation, satiation, other upper gastrointestinal hormones, or postprandial symptoms. Given these findings, a subset of patients with rapid gastric emptying (e.g., the estimated 20% of patients with functional dyspepsia) could be candidates for treatments that stimulate a secretin receptor such as sacubitril, which inhibits neprilysin, an enzyme that degrades secretin.

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Sartor, Daniela M., Arthur Shulkes, and Anthony J. M. Verberne. "An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 3 (March 2006): R625—R633. http://dx.doi.org/10.1152/ajpregu.00639.2005.

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Ingestion of a meal results in gastrointestinal (GI) hyperemia and is associated with systemic and paracrine release of a number of peptide hormones, including cholecystokinin (CCK) and 5-hydroxytryptamine (5-HT). Systemic administration of CCK octapeptide inhibits a subset of presympathetic neurons of the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor tone to the GI viscera. The aim of this study was to determine whether endogenous release of CCK and/or 5-HT also inhibits CCK-sensitive RVLM neurons. The effects of intraduodenal administration of the secretagogues sodium oleate (SO) and soybean trypsin inhibitor (SBTI) on circulating levels of CCK and 5-HT were examined. In separate experiments, the discharge rates of barosensitive, medullospinal, CCK-sensitive RVLM presympathetic vasomotor neurons were recorded after rapid intraduodenal infusion of SO-SBTI or water. Alternatively, animals were pretreated with the CCK1 receptor antagonists devazepide and lorglumide or the 5-HT3 antagonist MDL-72222 before SO-SBTI administration. Secretagogue infusion significantly increased the level of circulating CCK, but not 5-HT. SO-SBTI significantly decreased (58%) the neuronal firing rate of CCK-sensitive RVLM neurons compared with water (5%). CCK1 receptor antagonists did not reverse SO-SBTI-induced neuronal inhibition (58%), whereas the 5-HT3 antagonist significantly attenuated the effect (22%). This study demonstrates a functional relation between a subset of RVLM presympathetic vasomotor neurons and meal-related signals arising from the GI tract. It is likely that endogenously released 5-HT acts in a paracrine fashion on GI 5-HT3 receptors to initiate reflex inhibition of these neurons, resulting in GI vasodilatation by withdrawal of sympathetic tone.

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Prinz, Christian, Robert Zanner, Markus Gerhard, Sabine Mahr, Nina Neumayer, Barbara Höhne-Zell, and Manfred Gratzl. "The mechanism of histamine secretion from gastric enterochromaffin-like cells." American Journal of Physiology-Cell Physiology 277, no. 5 (November 1, 1999): C845—C855. http://dx.doi.org/10.1152/ajpcell.1999.277.5.c845.

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Enterochromaffin-like (ECL) cells play a pivotal role in the peripheral regulation of gastric acid secretion as they respond to the functionally important gastrointestinal hormones gastrin and somatostatin and neural mediators such as pituitary adenylate cyclase-activating peptide and galanin. Gastrin is the key stimulus of histamine release from ECL cells in vivo and in vitro. Voltage-gated K+ and Ca2+ channels have been detected on isolated ECL cells. Exocytosis of histamine following gastrin stimulation and Ca2+ entry across the plasma membrane is catalyzed by synaptobrevin and synaptosomal-associated protein of 25 kDa, both characterized as a soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein. Histamine release occurs from different cellular pools: preexisting vacuolar histamine immediately released by Ca2+ entry or newly synthesized histamine following induction of histidine decarboxylase (HDC) by gastrin stimulation. Histamine is synthesized by cytoplasmic HDC and accumulated in secretory vesicles by proton-histamine countertransport via the vesicular monoamine transporter subtype 2 (VMAT-2). The promoter region of HDC contains Ca2+-, cAMP-, and protein kinase C-responsive elements. The gene promoter for VMAT-2, however, lacks TATA boxes but contains regulatory elements for the hormones glucagon and somatostatin. Histamine secretion from ECL cells is thereby under a complex regulation of hormonal signals and can be targeted at several steps during the process of exocytosis.

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Yu, Defu, Weiyun Zhu, and Suqin Hang. "Effects of Long-Term Dietary Protein Restriction on Intestinal Morphology, Digestive Enzymes, Gut Hormones, and Colonic Microbiota in Pigs." Animals 9, no. 4 (April 20, 2019): 180. http://dx.doi.org/10.3390/ani9040180.

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Using protein-restriction diets becomes a potential strategy to save the dietary protein resources. However, the mechanism of low-protein diets influencing pigs’ growth performance is still controversial. This study aimed to investigate the effect of protein-restriction diets on gastrointestinal physiology and gut microbiota in pigs. Eighteen weaned piglets were randomly allocated to three groups with different dietary protein levels. After a 16-week trial, the results showed that feeding a low-protein diet to pigs impaired the epithelial morphology of duodenum and jejunum (p < 0.05) and reduced the concentration of many plasma hormones (p < 0.05), such as ghrelin, somatostatin, glucose-dependent insulin-tropic polypeptide, leptin, and gastrin. The relative abundance of Streptococcus and Lactobacillus in colon and microbiota metabolites was also decreased by extreme protein-restriction diets (p < 0.05). These findings suggested that long-term ingestion of a protein-restricted diet could impair intestinal morphology, suppress gut hormone secretion, and change the microbial community and fermentation metabolites in pigs, while the moderately low-protein diet had a minimal effect on gut function and did not impair growth performance.

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Steinert, Robert E., Christine Feinle-Bisset, Lori Asarian, Michael Horowitz, Christoph Beglinger, and Nori Geary. "Ghrelin, CCK, GLP-1, and PYY(3–36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB." Physiological Reviews 97, no. 1 (January 2017): 411–63. http://dx.doi.org/10.1152/physrev.00031.2014.

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The efficacy of Roux-en-Y gastric-bypass (RYGB) and other bariatric surgeries in the management of obesity and type 2 diabetes mellitus and novel developments in gastrointestinal (GI) endocrinology have renewed interest in the roles of GI hormones in the control of eating, meal-related glycemia, and obesity. Here we review the nutrient-sensing mechanisms that control the secretion of four of these hormones, ghrelin, cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), and peptide tyrosine tyrosine [PYY(3–36)], and their contributions to the controls of GI motor function, food intake, and meal-related increases in glycemia in healthy-weight and obese persons, as well as in RYGB patients. Their physiological roles as classical endocrine and as locally acting signals are discussed. Gastric emptying, the detection of specific digestive products by small intestinal enteroendocrine cells, and synergistic interactions among different GI loci all contribute to the secretion of ghrelin, CCK, GLP-1, and PYY(3–36). While CCK has been fully established as an endogenous endocrine control of eating in healthy-weight persons, the roles of all four hormones in eating in obese persons and following RYGB are uncertain. Similarly, only GLP-1 clearly contributes to the endocrine control of meal-related glycemia. It is likely that local signaling is involved in these hormones' actions, but methods to determine the physiological status of local signaling effects are lacking. Further research and fresh approaches are required to better understand ghrelin, CCK, GLP-1, and PYY(3–36) physiology; their roles in obesity and bariatric surgery; and their therapeutic potentials.

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Furness, John B., Wolfgang A. A. Kunze, and Nadine Clerc. "II. The intestine as a sensory organ: neural, endocrine, and immune responses." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 5 (November 1, 1999): G922—G928. http://dx.doi.org/10.1152/ajpgi.1999.277.5.g922.

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The lining of the gastrointestinal tract is the largest vulnerable surface that faces the external environment. Just as the other large external surface, the skin, is regarded as a sensory organ, so should the intestinal mucosa. In fact, the mucosa has three types of detectors: neurons, endocrine cells, and immune cells. The mucosa is in immediate contact with the intestinal contents so that nutrients can be efficiently absorbed, and, at the same time, it protects against the intrusion of harmful entities, such as toxins and bacteria, that may enter the digestive system with food. Signals are sent locally to control motility, secretion, tissue defense, and vascular perfusion; to other digestive organs, for example, to the stomach, gallbladder, and pancreas; and to the central nervous system, for example to influence feeding behavior. The three detecting systems in the intestine are more extensive than those of any other organ: the enteric nervous system contains on the order of 108 neurons, the gastroenteropancreatic endocrine system uses more than 20 identified hormones, and the gut immune system has 70– 80% of the body's immune cells. The gastrointestinal tract has an integrated response to changes in its luminal contents. When this response is maladjusted or is overwhelmed, the consequences can be severe, as in cholera intoxication, or debilitating, as in irritable bowel syndrome. Thus it is essential to obtain a full understanding of the sensory functions of the intestine, of how the body reacts to the information, and of how neural, hormonal, and immune signals interact.

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Ramos-Alvarez, Irene, and R. T. Jensen. "P21-activated kinase 4 in pancreatic acinar cells is activated by numerous gastrointestinal hormones/neurotransmitters and growth factors by novel signaling, and its activation stimulates secretory/growth cascades." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 2 (August 1, 2018): G302—G317. http://dx.doi.org/10.1152/ajpgi.00005.2018.

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p21-activated kinases (PAKs) are highly conserved serine/threonine protein kinases, which are divided into two groups: group-I (PAKs1–3) and group-II (PAKs4–6). In various tissues, Group-II PAKs play important roles in cytoskeletal dynamics and cell growth as well as neoplastic development/progression. However, little is known about Group-II PAK’s role in a number of physiological events, including their ability to be activated by gastrointestinal (GI) hormones/neurotransmitters/growth factors (GFs). We used rat pancreatic acini to explore the ability of GI hormones/neurotransmitters/GFs to activate Group-II-PAKs and the signaling cascades involved. Only PAK4 was detected in pancreatic acini. PAK4 was activated by endothelin, secretagogues-stimulating phospholipase C (bombesin, CCK-8, and carbachol), by pancreatic GFs (insulin, insulin-like growth factor 1, hepatocyte growth factor, epidermal growth factor, basic fibroblast growth factor, and platelet-derived growth factor), and by postreceptor stimulants (12-O-tetradecanoylphobol-13-acetate and A23187 ). CCK-8 activation of PAK4 required both high- and low-affinity CCK1-receptor state activation. It was reduced by PKC-, Src-, p44/42-, or p38-inhibition but not with phosphatidylinositol 3-kinase-inhibitors and only minimally by thapsigargin. A protein kinase D (PKD)-inhibitor completely inhibited CCK-8-stimulated PKD-activation; however, stimulated PAK4 phosphorylation was only inhibited by 60%, demonstrating that it is both PKD-dependent and PKD-independent. PF-3758309 and LCH-7749944, inhibitors of PAK4, decreased CCK-8-stimulated PAK4 activation but not PAK2 activation. Each inhibited ERK1/2 activation and amylase release induced by CCK-8 or bombesin. These results show that PAK4 has an important role in modulating signal cascades activated by a number of GI hormones/neurotransmitters/GFs that have been shown to mediate both physiological/pathological responses in acinar cells. Therefore, in addition to the extensive studies on PAK4 in pancreatic cancer, PAK4 should also be considered an important signaling molecule for pancreatic acinar physiological responses and, in the future, should be investigated for a possible role in pancreatic acinar pathophysiological responses, such as in pancreatitis. NEW & NOTEWORTHY This study demonstrates that the only Group-II p21-activated kinase (PAK) in rat pancreatic acinar cells is PAK4, and thus differs from islets/pancreatic cancer. Both gastrointestinal hormones/neurotransmitters stimulating PLC and pancreatic growth factors activate PAK4. With cholecystokinin (CCK), activation is PKC-dependent/-independent, requires both CCK1-R affinity states, Src, p42/44, and p38 activation. PAK4 activation is required for CCK-mediated p42/44 activation/amylase release. These results show PAK4 plays an important role in mediating CCK physiological signal cascades and suggest it may be a target in pancreatic acinar diseases besides cancer.

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Seidel, E. R., and R. G. Snyder. "Pentagastrin induction of spermine/spermidine N1-acetyltransferase and mucosal polyamines." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 1 (January 1, 1989): G16—G21. http://dx.doi.org/10.1152/ajpgi.1989.256.1.g16.

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The trophic response of the gastrointestinal mucosa to treatment with the hormone gastrin includes a polyamine-dependent step. Because gastrin does not induce ornithine decarboxylase, experiments were designed to determine whether pentagastrin induced the polyamine interconverting enzyme, spermine/spermidine N1-acetyltransferase (SAT). Eight hours after intraperitoneal treatment of rats with either spermidine (0.8 mmol/kg) or pentagastrin (250 micrograms/kg) oxyntic gland mucosal SAT activity was increased from roughly 400 to 800 pmol [14C]acetate.mg protein-1.h-1. In contrast, colonic mucosa was not sensitive to pentagastrin even though spermidine treatment induced nearly a 400% increase in SAT activity. Measurement of both oxyntic gland and colonic mucosal polyamine concentrations showed that by 16 h after pentagastrin (250 micrograms/kg ip) putrescine, acetylspermidine, and spermidine levels all were increased to a level approximately 200% of that observed in NaCl-treated rats. By 24 h mucosal polyamine content of pentagastrin-treated rats was not different from control. Essentially the same results were found in animals treated with difluoromethylornithine, thus demonstrating that the increase in mucosal polyamine concentration was not related to the induction of ornithine decarboxylase. The results of these experiments demonstrate that unlike most hormones, the hormone gastrin induces the polyamine converting enzyme, SAT, rather than ornithine decarboxylase during stimulation of polyamine-dependent cell growth and/or division.

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Kolek, Olga I., Eric R. Hines, Marci D. Jones, Loren K. LeSueur, Maciej A. Lipko, Pawel R. Kiela, James F. Collins, Mark R. Haussler, and Fayez K. Ghishan. "1α,25-Dihydroxyvitamin D3 upregulates FGF23 gene expression in bone: the final link in a renal-gastrointestinal-skeletal axis that controls phosphate transport." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 6 (December 2005): G1036—G1042. http://dx.doi.org/10.1152/ajpgi.00243.2005.

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Fibroblast growth factor (FGF)23 is a phosphaturic hormone that decreases circulating 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] and elicits hypophosphatemia, both of which contribute to rickets/osteomalacia. It has been shown recently that serum FGF23 increases after treatment with renal 1,25(OH)2D3 hormone, suggesting that 1,25(OH)2D3 negatively feedback controls its levels by inducing FGF23. To establish the tissue of origin and the molecular mechanism by which 1,25(OH)2D3 increases circulating FGF23, we administered 1,25(OH)2D3 to C57BL/6 mice. Within 24 h, these mice displayed a dramatic elevation in serum immunoreactive FGF23, and the expression of FGF23 mRNA in bone was significantly upregulated by 1,25(OH)2D3, but there was no effect in several other tissues. Furthermore, we treated rat UMR-106 osteoblast-like cells with 1,25(OH)2D3, and real-time PCR analysis revealed a dose- and time-dependent stimulation of FGF23 mRNA concentrations. The maximum increase in FGF23 mRNA was 1,024-fold at 10−7 M 1,25(OH)2D3 after 24-h treatment, but statistically significant differences were observed as early as 4 h after 1,25(OH)2D3 treatment. In addition, using cotreatment with actinomycin D or cycloheximide, we observed that 1,25(OH)2D3 regulation of FGF23 gene expression occurs at the transcriptional level, likely via the nuclear vitamin D receptor, and is dependent on synthesis of an intermediary transfactor. These results indicate that bone is a major site of FGF23 expression and source of circulating FGF23 after 1,25(OH)2D3 administration or physiological upregulation. Our data also establish FGF23 induction by 1,25(OH)2D3 in osteoblasts as a feedback loop between these two hormones that completes a kidney-intestine-bone axis that mediates phosphate homeostasis.

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Davis, M. S., K. W. Hinchcliff, K. K. Williamson, E. C. McKenzie, and C. M. Royer. "Effect of multiday exercise on serum hormones and metabolic substrate concentrations in racing sled dogs." Comparative Exercise Physiology 16, no. 3 (March 23, 2020): 197–205. http://dx.doi.org/10.3920/cep190068.

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Prolonged submaximal exercise relies on the steady delivery of oxidizable substrates to the working muscle, with the sources of those substrates either stored reserves or food absorbed from the gastrointestinal tract during exercise. Fat oxidation could be advantageous for this type of exercise because of potentially greater reserves, but recent studies suggest that athletic dogs remain highly dependent on carbohydrate to fuel exercise despite ingesting a high fat diet. The purpose of this study was to characterise the pattern of exercise-induced hormone and substrate concentrations as they relate to carbohydrate and fat metabolism during prolonged submaximal exercise in dogs. Two studies (a 10-dog pilot study and a subsequent primary study using 54 Alaskan sled dogs) were conducted with the dogs running 160 km/day for 4 or 5 days. Blood samples were obtained within 60 min of cessation of daily exercise and in the second study within 30 min of the start of the next day of exercise. Samples were analysed for key hormones and substrates. Results demonstrated the development of a strong hormonal stimulus for glycogenolysis/gluconeogenesis that coincided with sparing and replenishment of muscle glycogen. The stimulus for glycogenolysis/gluconeogenesis tended to diminish during rest periods in the early stages of the exercise challenge, but remained increased during later rest periods and for several days after the conclusion of exercise. These data support the hypothesis that in the face of a high-fat diet, ultra-endurance racing sled dogs rely on large amounts of hepatic glucose output to support prolonged submaximal exercise.

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Journal articles on the topic 'Gastrointestinal hormones Physiology'

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