Relevant bibliographies by topics / Hormones gastrointestinales

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Academic literature on the topic 'Hormones gastrointestinales'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 July 2024

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Journal articles on the topic "Hormones gastrointestinales"

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REHFELD, JENS F. "The New Biology of Gastrointestinal Hormones." Physiological Reviews 78, no. 4 (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 (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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Mai, Yang, Francesca K. H. Gavins, Liu Dou, et al. "A Non-Nutritive Feeding Intervention Alters the Expression of Efflux Transporters in the Gastrointestinal Tract." Pharmaceutics 13, no. 11 (2021): 1789. http://dx.doi.org/10.3390/pharmaceutics13111789.

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Intestinal interactions with nutrients, xenobiotics and endogenous hormones can influence the expression of clinically relevant membrane transporters. These changes in the gastrointestinal (GI) physiology can in turn affect the absorption of numerous drug substrates. Several studies have examined the effect of food on intestinal transporters in male and female humans and animal models. However, to our knowledge no studies have investigated the influence of a non-nutritive fibre meal on intestinal efflux transporters and key sex and GI hormones. Here, we show that a fibre meal increased the acute expression of P-glycoprotein (P-gp), breast cancer resistance protein (BCRP), and multidrug-resistance-associated protein-2 (MRP2) in small intestinal segments in both male and female Wistar rats. Enzyme-linked immunosorbent assays were used for the protein quantification of efflux transporters and hormonal plasma concentration. In male rats, the fibre meal caused the plasma concentration of the GI hormone cholecystokinin (CCK) to increase by 75% and the sex hormone testosterone to decrease by 50%, whereas, in contrast, the housing food meal caused a decrease in CCK by 32% and testosterone saw an increase of 31%. No significant changes in the hormonal concentrations, however, were seen in female rats. A deeper understanding of the modulation of efflux transporters by sex, food intake and time can improve our understanding of inter- and intra-variability in the pharmacokinetics of drug substrates.
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Idrovo, Juan-Pablo, Jill A. Shults, Brenda J. Curtis, Michael M. Chen, and Elizabeth J. Kovacs. "Alcohol Intoxication and the Postburn Gastrointestinal Hormonal Response." Journal of Burn Care & Research 40, no. 6 (2019): 785–91. http://dx.doi.org/10.1093/jbcr/irz083.

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Abstract Gastrointestinal hormones are essential in postburn metabolism. Since near 50% of burn victims test positive for blood alcohol levels at hospital admission and have inferior outcomes compared to nonintoxicated burn patients; we hypothesized that the gastrointestinal hormone secretion is compromised in intoxicated burn victims. To test our theory, we quantified gastrointestinal hormones serum levels in a combine ethanol intoxication and burn injury mouse model. Thus, mice received a daily dose of ethanol for 3 days, rested 4 days, and were given ethanol 3 additional days. Mice underwent 15% TBSA scald burn 30 minutes after their last ethanol dose. Serum samples were collected 24 hours after burn injury. Nonintoxicated burned mice exhibited an increase in glucose, insulin, ghrelin, plasminogen activator inhibitor-1, leptin, and resistin by 1.4-, 3-, 13.5-, 6.2-, 9.4-, and 2.4-fold, respectively, compared to sham vehicle mice (P < .05). Burn injury also reduced serum gastric inhibitory polypeptide (GIP) by 32% compared to sham-injured, vehicle-treated mice. Leptin, resistin, glucagon-like peptide-1, as well as insulin, were not different from sham groups when intoxication preceded burn injury. Nevertheless, in burned mice treated with ethanol, gastric inhibitory polypeptide and glucagon serum levels exhibited a significant fold increase of 3.5 and 4.7, respectively. With these results, we conclude that 24 hours after burn injury, mice developed significant changes in gastrointestinal hormones, along with hyperglycemia. Moreover, the combined insult of burn and ethanol intoxication led to additional hormonal changes that may be attributed to a potential pancreatic dysfunction. Further multiday studies are required to investigate the etiology, behavior, and clinical significance of these hormonal changes.
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Somogyi, V., A. Gyorffy, T. J. Scalise, et al. "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 (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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Liddle, R. A. "Regulation of cholecystokinin secretion by intraluminal releasing factors." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 3 (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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Sharman‐Koendjbiharie, Meenakoemarie, Wim P. M. Hopman, Marjolein Piena‐Spoel, Marcel J. I. J. Albers, Jan B. M. J. Jansen, and Dick Tibboel. "Gut Hormones in Preterm Infants With Necrotizing Enterocolitis During Starvation and Reintroduction of Enteral Nutrition." Journal of Pediatric Gastroenterology and Nutrition 35, no. 5 (2002): 674–79. http://dx.doi.org/10.1002/j.1536-4801.2002.tb07928.x.

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ABSTRACTObjectivesGastrointestinal hormones control gut functions in response to enteral nutrition. Diseases involving the gastrointestinal tract, such as necrotizing enterocolitis, may affect gut hormone secretion and therefore influence gut functions. Because bowel rest is an important part of the treatment, infants with this disease are especially at risk for an altered gut hormone secretion and thus for compromised gut functions.MethodsIn the current study, the gastrointestinal hormone profiles of eight preterm infants with an ileostomy after necrotizing enterocolitis (Bell stages 2 and 3) were evaluated during starvation and reintroduction of enteral nutrition. Basal and postprandial plasma concentrations of gastrin, cholecystokinin, and peptide YY were measured with sensitive and specific radioimmunoassays. The results were compared with those of 11 controls.ResultsIn the patients and the controls, plasma concentrations of all hormones were higher postprandially. The increases in cholecystokinin and peptide YY were significant in the patients. Compared with the controls, all concentrations were higher in the patients, and changes were significant for basal and postprandial cholecystokinin and postprandial peptide YY.ConclusionsEnteral nutrition stimulates the secretion of gastrointestinal hormones, also in premature infants with a diseased distal small bowel and colon, as in necrotizing enterocolitis. The postprandial increase of peptide YY in patients with an ileostomy indicates that enteral substrate in the colon is not necessary for stimulation of peptide YY secretion.
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Romero Suárez, Tatiana Lissett, Juan José Reyes Vélez, Henry Wellington Calderón Cornejo, Anllelyne Elizabeth Gorozabel Alman, and María Nikolle Intriago Freire. "Rol neuroendocrino del sistema gastrointestinal." Anatomía Digital 6, no. 3.1 (2023): 59–73. http://dx.doi.org/10.33262/anatomiadigital.v6i3.1.2656.

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Introducción: el sistema gastrointestinal, más lejos de su clásico rol en la alimentación e inmunidad, cumple también funciones endocrinas mediante la secreción de hormonas que participan en la homeostasis. Objetivo: exponer las generalidades del rol neuroendocrino del sistema gastrointestinal y su impacto en la homeostasis. Métodos: revisión narrativa de la literatura que incluyó 46 artículos seleccionados en base a su disponibilidad abierta y ser publicados en inglés y español. Conclusiones: el estudio de las hormonas gastrointestinales permite el desarrollo de nuevas tecnologías diagnósticas y dianas de tratamiento en el contexto de distintas patologías. Conocer el rol de estas hormonas, desde el prisma de las ciencias biomédicas, podría aportar en el tratamiento de patologías como diabetes, obesidad y síndrome metabólico.
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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 (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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Harty, Richard F. "Gastrointestinal hormones." Current Opinion in Gastroenterology 7, no. 6 (1991): 906–12. http://dx.doi.org/10.1097/00001574-199112000-00012.

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Dissertations / Theses on the topic "Hormones gastrointestinales"

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Nicol, Philippe. "Peptides C-terminaux de la sorbine : pharmacocinétique, formes circulantes, recherche des mécanismes d'action." Lyon 1, 1996. http://www.theses.fr/1996LYO1T077.

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Plaisancie, Pascale. "Modulation de la sécrétion du peptide YY et du peptide glucagon-like 1 tronqué : étude à partir d'un modèle de côlon isolé vascularisé de rat." Lyon 1, 1994. http://www.theses.fr/1994LYO1T240.

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Hollanda, Ramírez Ana M. de. "Adaptación metabólica y variabilidad en la pérdida de peso tras la cirugía bariátrica." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/398897.

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La obesidad mórbida es un problema de salud creciente. La cirugía bariátrica es actualmente el tratamiento más eficaz para la pérdida de peso, sin embargo esta pérdida de peso es súmamente variable. En alrededor del 20% de los pacientes intervenidos la pérdida de peso es insuficiente, las causas de esta gran variabilidad no están bien definidas. Las hipótesis planteadas en esta tesis son las siguientes, 1. La variabilidad en la pérdida de peso tras la cirugía bariátrica puede ilustrarse en un número limitado de trayectorias ponderales con significación clínica. 2. La variabilidad en la pérdida de peso puede explicarse por lo menos en parte por la variabilidad en el efecto de las hormonas gastrointestinales. Los objetivos son los siguientes, 1. Describir la presencia de diferentes patrones de pérdida de peso en una cohorte de individuos operados mediante bypass gástrico y gastrectomía vertical con 5 años de seguimiento y evaluar los predictores clínicos de cada trayectoria ponderal. 2. Comparar la respuesta de las hormonas gastrointestinales en los grupos de fracaso y éxito en la pérdida de peso tras el bypass gástrico. 3. Comparar los niveles plasmáticos de citrina, marcador de la masa entérica, en los grupos de fracaso y éxito en la pérdida de peso tras el bypass gástrico. 4. Valorar el rol causal de las hormonas gastrointestinales sobre la ingesta y su repercusión sobre la respuesta ponderal en los diferentes grupos de fracaso y éxito tras el bypass gástrico a través del bloqueo de la secreción de hormonas gastrointestinales con octreótido. Los resultados y conclusiones derivadas de esta tesis se resumen en los siguientes puntos, 1- La cirugía bariátrica logra una pérdida de peso muy variable, sus efectos se atenúan y su variabilidad aumenta con el transcurso del tiempo. 2. Se pueden identificar dos trayectorias clínicamente diferentes en los que presentan escasa pérdida de peso. El fracaso primario ó resistencia a la pérdida de peso y, el fracaso secundario o mayor tendencia a reganancia de peso. 3. La cirugía bariátrica se asocia una menor pérdida del exceso de peso en los pacientes con obesidad extrema. 4. El mayor cumplimiento de las visitas de seguimiento se asocia con mayor respuesta a la cirugía bariátrica. 5. El bypass y la gastrectomía vertical consiguen resultados similares a corto y mediano plazo, sin embargo la gastrectomía vertical se asocia con mayor reganancia ponderal a medio plazo. 6. El éxito en la pérdida de peso tras el bypass gástrico se asocia a un perfil hormonal más anorexígeno en comparación con el fracaso. 7. Las hormonas gastrointestinales ejercen un papel importante en el control fisiológico de la ingesta calórica también tras el BPG. 8. Las hormonas gastrointestinales no juegan un papel crítico en las diferencias en la ingesta entre personas con éxito o fracaso secundario en la pérdida de peso tras el bypass gástrico. 9. Tras el bypass gástrico sucede una adaptación intestinal que es progresiva en el tiempo. 10. Los datos disponibles sugieren que la adaptación intestinal no ejerce un rol determinante del éxito en la pérdida de peso tras el bypass gástrico.<br>Morbidly obesity is a growing health problem. Bariatric surgery is currently the most effective treatment for weight loss, however its results are highly variable. In about 20% of individuals weight loss is insufficient, the causes of this high variability are not well defined. The hypotheses made in this thesis are as follows, 1. Variability in weight loss after bariatric surgery can be illustrated in a limited number of weight loss patterns with clinical significance. 2. Variability in weight loss can be explained at least partly by the effect of variability in the gastrointestinal hormones. The aims were to, 1. Describe the presence of different patterns of weight loss in a cohort of individuals operated by gastric bypass and vertical gastrectomy with 5 years of follow up and evaluate clinical predictors of each weight loss path. 2. Compare the response of gastrointestinal hormones in groups of failure and success in weight loss after gastric bypass. 3. Compare the plasma levels of citrulline, marker enteric mass in groups of failure and success in weight loss after gastric bypass. 4. Assess the causal role of gastrointestinal hormones on food intake and its impact on the weight response in different groups of failure and success after gastric bypass by blocking the secretion of gastrointestinal hormones with octreotide. The results and conclusions from this thesis are summarized in the following points, 1- Bariatric surgery achieves weight loss with high variability, its effects are mitigated and variability increases with the passage of time. 2. We can identify two clinically different paths in those with low weight loss. The primary failure or resistance to weight loss, and secondary failure or greater tendency to regain weight. 3. Bariatric surgery is associated with a lower loss of excess weight in patients with extreme obesity. 4. Greater compliance with follow-up visits is associated with increased response to bariatric surgery. 5. The bypass and vertical gastrectomy get similar short and medium term results, however gastrectomy is associated with increased weight regain at medium term. 6. Successful weight loss after gastric bypass is associated with a more anorectic hormone profile compared with failure. 7. The gastrointestinal hormones play an important role in the physiological control of calorie intake also after gastric bypass. 8. Gastrointestinal hormones do not play a critical role in the differences in intake among people with secondary success or failure in weight loss after gastric bypass. 9. After gastric bypass intestinal adaptation occurs, it is progressive over time. 10. The available data suggest that intestinal adaptation does not play a decisive role to success in weight loss after gastric bypass.
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Saifia, Soumaya. "Mécanismes de sécrétion du peptide YY et du peptide glucagon-like 1 tronqué à partir de cellules intestinales natives isolées de rat." Lyon 1, 1997. http://www.theses.fr/1997LYO1T105.

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Smiri, Youssef. "Caractérisation et purification de molécules apparentées à la gastrine/cholécystokinine chez une annélide polychète, nereis diversicolor." Lille 1, 1990. http://www.theses.fr/1990LIL10056.

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Ainsi que l'avaient démontré les travaux immunohistochimiques antérieurs, de nombreuses cellules du cerveau, du ganglion sous-sophagien et de la chaîne nerveuse de nereis diversicolor, présentent une immunoréactivité anti-gastrine/cck. Dans le cadre de ce travail, notre objectif était de caractériser et de purifier le ou les peptide(s) de nereis apparenté(s) à la gastrine/cck de mammifères. L'étude a été réalisée en partie sur des prostomiums isolés renfermant le cerveau, en partie sur des corps entiers et ce, en réalisant différentes étapes chromatographiques suivies chacune d'un test ria. La caractérisation de la molécule a été entreprise en utilisant différents anticorps spécifiques de la partie commune c-terminale de la gastrine et de la cck ou de la seule gastrine. Nos résultats permettent de conclure que les peptides recherchés ne présentent pas d'homologie avec la gastrine en dehors du pentapeptide c-terminal. Les études réalisées à partir de prostomiums isolés ou de corps entiers démontrent également que plusieurs molécules sont reconnues lors des tests ria. Il s'agit vraisemblablement de différentes formes issues d'un même précurseur comme le sont les différentes formes moléculaires de cck provenant de la maturation de la pro-cck. Ainsi donc, chez les annélides, le matériel apparenté à la gastrine/cck des mammifères apparaît hétérogène. Cependant, comme l'une des fractions renferme à elle seule près de 40% de l'immunoréactivite totale, il est désormais possible, en utilisant le procédé de purification mis au point, d'analyser la forme majeure du peptide apparenté à la gastrine/cck des néréidiens
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Dumoulin, Valérie. "Modulation de la sécrétion de la neurotensine, du peptide YY et du peptide glucagon-like 1 tronqué : étude à partir d'un modèle d'intestin isolé vascularisé de rat." Lyon 1, 1996. http://www.theses.fr/1996LYO1T158.

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Devin, Chantal. "Synthèse et étude pharmacologique d'analogues peptidiques et pseudopeptidiques de la bombésine." Montpellier 2, 1997. http://www.theses.fr/1997MON20031.

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Ce travail est consacre a la synthese et a l'etude pharmacologique d'analogues peptidiques et pseudopeptidiques de la bombesine. Une etude sur les relations structure-activite de la bombesine (bn) a ete developpee. Dans un premier temps, nous avons synthetise des analogues modifies au niveau du nonapeptide c-terminal par substitution d'aminoacides et introduction de liaisons pseudopeptidiques. L'introduction de liaisons hydroxyamides au niveau de la partie c-terminale a conduit a de puissants antagonistes sur la secretion d'amylase pancreatique induite par la bombesine et sur la proliferation cellulaire des fibroblastes swiss 3t3 de souris. Dans un deuxieme temps, nous avons synthetise des analogues cycliques et dimerises de la bombesine. La derniere partie de ce travail a ete la synthese d'analogues de la bombesine etendue du cote c-terminal par un residu glycine. Certains de ces analogues sont de puissants agonistes sur la proliferation cellulaire des fibroblastes swiss 3t3 de souris. Ces composes devraient nous permettre de savoir s'il existe des recepteurs specifiques de ces formes glycine etendue et si ces recepteurs sont impliques dans la proliferation cellulaire des fibroblastes swiss 3t3 de souris
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Vilardaga, Jean-Pierre. "Contribution à l'étude des récepteurs aux hormones gastrointestinales: relation structure-activité du récepteur de la sécrétine." Doctoral thesis, Universite Libre de Bruxelles, 1996. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212413.

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Briet, Christian. "Synthèse et propriétés biologiques de nouveaux analogues peptidiques de la cholecystokinine et de la gastrine : étude de l'importance des résidus C-terminaux." Montpellier 2, 1986. http://www.theses.fr/1986MON20041.

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Cette etude porte sur les relations structure-activite dans l'heptapeptide c-terminal responsable de l'activite biologique de la cholecystokinine (cck); en particulier, nos syntheses ont porte sur les acides amines en position 32 et 33. Ces syntheses ont ete effectuees en phase liquide par la methode des esters actives ou grace au reactif de castro (b. O. P. ). La suppression de la phenylalanine en position 33 conduit a un analogue antagoniste des recepteurs de la cck: la cck-27-32-nh::(2). Ce compose nous a amene a elaborer toute une famille de tri- et tetrapeptides qui inhibent la secretion acide induite par la gastrine, hormone apparentee a la cck. Par cette etude on a mis en evidence le role fondamental du residu c-terminal de la cck pour l'activite biologique intrinseque de la cck et de la gastrine
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Bobo, Marie-Hélène. "Approche pharmacologique de l'homéostasie calcique dans la cellule musculaire lisse gastrique." Montpellier 1, 1994. http://www.theses.fr/1994MON13503.

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Books on the topic "Hormones gastrointestinales"

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A, Alemayehu, and Brown David R. 1954-, eds. Gastrointestinal regulatory peptides. Springer-Verlag, 1993.

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1954-, Brown David R., ed. Gastrointestinalregulatory peptides. Springer-Verlag, 1993.

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A, Johnston Craig, and Barnes Charles D. 1935-, eds. Brain-gut peptides and reproductive function. CRC Press, 1991.

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1940-, Blázquez E., ed. Gut regulatory peptides: Their role in health and disease. Karger, 1987.

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How gut and brain control metabolism. Karger, 2014.

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1928-, Thompson James C., ed. Gastrointestinal endocrinology. McGraw-Hill, 1987.

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D, Morisset Jean Ph, and Solomon Travis E, eds. Growth of the gastrointestinal tract: Gastrointestinal hormones and growth factors. CRC Press, 1991.

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E, Daniel E., ed. Neuropeptide function in the gastrointestinal tract. CRC Press, 1991.

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S, Radbilʹ O., ред. Gormony pishchevaritelʹnoĭ sistemy: Fiziologii͡a︡, patologii͡a︡, teorii͡a︡ funkt͡s︡ionalʹnykh blokov. "Nauka", 1995.

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1939-, Cohen Sidney, and Soloway Roger D, eds. Hormone-producing tumors of the gastrointestinal tract. Churchill Livingstone, 1985.

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Book chapters on the topic "Hormones gastrointestinales"

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Desbuquois, Bernard, Elisabeth Granström, Pär Westlund, and Bengt Samuelson. "Gastrointestinal Hormones." In Hormones. Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-011-3060-8_12.

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

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Arnold, R., and H. Koop. "Gastrointestinale Hormone." In Interdisziplinäre Gastroenterologie. Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70522-9_39.

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Grandt, D., V. Eysselein, and H. Goebell. "Gastrointestinale Hormone." In Endokrinologie des Kindes- und Jugendalters. Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-59043-6_10.

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Guo, Yan-Shi, and Courtney M. Townsend. "Gastrointestinal Hormones and Gastrointestinal Cancer Growth." In Gastrointestinal Endocrinology. Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-695-9_8.

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Wang, Yan, and Efi Kokkotou. "Gastrointestinal Hormones and Obesity." In Metabolic Basis of Obesity. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1607-5_6.

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Miller, Laurence J. "Gastrointestinal Hormones and Receptors." In Yamada' s Textbook of Gastroenterology. John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118512074.ch13.

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Prodam, Flavia, Simonetta Bellone, Silvia Savastio, et al. "Hormones and Gastrointestinal Function." In Neonatology. Springer Milan, 2012. http://dx.doi.org/10.1007/978-88-470-1405-3_43.

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Ko, Tien C., and James C. Thompson. "Effects of Aging on Gut Hormones." In Gastrointestinal Endocrinology. Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-695-9_7.

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Becker, H. D. "Dumpingsyndrom und gastrointestinale Hormone." In Stand und Gegenstand chirurgischer Forschung. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70648-6_29.

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Conference papers on the topic "Hormones gastrointestinales"

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Elbashir, Israa, Heba Al Khatib, and Hadi Yassine. "Replication Dynamics, Pathogenicity, and Evolution of Influenza Viruses in Intestinal Caco-2 Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0166.

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Background: Influenza virus is a major cause of respiratory infections worldwide. Besides the common respiratory symptoms, namouras cases with gastrointestinal symptoms have been reported. Moreover, influenza virus has been detected in feces of up to 20.6 % of influenza-infected patients. Therefore, direct infection of intestinal cells with influenza virus is suspected; however, the mechanism of this infection has not been explored. AIM: To investigate influenza virus replication, cellular responses to infection, and virus evolution following serial infection in human Caucasian colon adenocarcinoma cells (Caco-2 cells). Method: Two influenza A subtypes (A/H3N2 and A/H1N1pdm 09) and one influenza B virus (B/Yamagata) were serially passaged in Caco-2. Quantitative PCR was used to study hormones and cytokines expression following infection. Deep sequencing analysis of viral genome was used to assess the virus evolution. Results: The replication capacity of the three viruses was maintained throughout 12 passages, with H3N2 virus being the fastest in adaptation. The expression of hormone and cytokines in Caco-2 cells was considerably different between the viruses and among the passages, however, a pattern of induction was observed at the late phase of infection. Deep sequencing analysis revealed a few amino acid substitutions in the HA protein of H3N2 and H1N1 viruses, mostly in the antigenic site. Moreover, virus evolution at the quasispecies level based on HA protein revealed that H3N2 and H1N1 harbored more diverse virus populations when compared to IBV, indicating their higher evolution within Caco-2 cells. Conclusion: The findings of this study indicate the possibility of influenza virus replication in intestinal cells. To further explain the gastrointestinal complications of influenza infections in-vivo experiments with different influenza viruses are needed.
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Al-Asmar, Jawaher, Sara Rashwan, and Layla Kamareddine. "The use of Drosophila Melanogaster as a Model Organism to study the effect of Bacterial Infection on Host Survival and Metabolism." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0186.

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Enterobacteriaceae, a large family of facultative anaerobic bacteria, encloses a broad spectrum of bacterial species including Escherichia coli, Salmonella enterica, and Shigella sonnei, that produce enterotoxins and cause gastrointestinal tract diseases. While much is known about the regulation and function of enterotoxins within the intestine of the host; the lack of cheap, practical, and genetically tractable model organisms has restricted the investigation of others facets of this host-pathogen interaction. Our group, among others, has employed Drosophila melanogaster, as a model organism to shed more light on some aspects of host-pathogen interplays. In this project, we addressed the effect of Escherichia coli, Salmonella enterica, and Shigella sonnei infection on altering the metabolic homeostasis of the host. Drosophila melanogaster flies were orally infected with Escherichia coli, Salmonella enterica, or Shigella sonnei, a method that mimics the natural route used by enteric pathogens to gain access to the gastrointestinal tract in humans. The results of our study revealed that both Escherichia coli and Shigella sonnei pathogens were capable of colonizing the host gut, resulting in a reduction in the life span of the infected host. Escherichia coli and Shigella sonnei infected flies also exhibited altered metabolic profiles including lipid droplets deprivation from their fat body (normal lipid storage organ in flies), irregular accumulation of lipid droplets in their gut, and significant elevation of systemic glucose and triglyceride levels. These metabolic alterations could be mechanistically attributed to the differential down-regulation in the expression of metabolic peptide hormones (Allatostatin A, Diuretic hormone 31, and Tachykinin) detected in the gut of Escherichia coli and Shigella sonnei infected flies. Salmonella enterica; however, was unable to colonize the gut of the host; and therefore, Salmonella enterica infected flies exhibited a relatively normal metabolic status as that of non infected flies. Gaining a proper mechanistic understanding of infection-induced metabolic alterations helps in modulating the pathogenesis of gastrointestinal tract diseases in a host and opens up for promising therapeutic approaches for infection induced metabolic disorders
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Pinheiro, Amanda Pereira Sindeaux, Pedro Vitor Ferreira Rodrigues, Raoni de Oliveira da Silva Domingues, and Leonardo José Rodrigues Araújo Melo. "Gastrointestinal dysmotility associated with Parkinson’s disease’s mechanism." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.461.

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Introduction: Parkinson’s Disease (PD) is a condition of the brain that consiste of the death of dopaminergic neurons in the substantia nigra, therefore causing dyskinesias and dystonias. Besides the motor symptoms, the neurogastro motility is affected by the disease, since gastrointestinal dysfunction is a frequent and clinically relevant symptom of PD. Objectives: To link the neural pathways and neurotransmitters that involve the neuroenteric system control and the PD’s pathology. Methods: A systematic literature review was performed based on data extraction through the advanced research engine from Pubmed. Publications with the descriptors “dysmotility” OR “gastro motility” AND “Parkinson” were selected. Results: Through clinical and pre-clinical studies on PD, there has been hypothesized a gut-brain axis that is connected through hormones, neurotransmitters and dopamanergic inputs. This hypothesis is supported by evidence in the showing of accumulation of alpha-synuclein in the vagal system and Enteric Nervous System, the use of drugs such as peripheral dopaminergic blockers and serotonin for gastroparesis, the ghrelin effects on the central dopaminergic system through modulation of the mesencephalic dopaminergic signaling tested on rats, the gastrointestinal autonomic neuropathy detected in PD patients and the establishment of gut dysmotility before motor onset symptoms. Therefore, dysmotility isues such as delayed gastric emptying may not only be a symptom of PD, but also contrubute to the pathogenesis itself through impaired signaling. Conclusion: The gut-brain axis can be not only a tool for PD diagnosis but also a treatment target to restrain the advance of the disease. Although many articles are related this subject, there is a lack of designed trials for atypical movement disorders. To explore the dysmotility in PD, there is a need for multi-modality standardized tests to evaluate severity and prevalence.
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Pogodaeva, P. S. "Changes in the parameters of a clinical blood test in rats using hypoglycemic agents for the potentiation of drugs with a hepatoprotective effect." In SPbVetScience. FSBEI HE St. Petersburg SUVM, 2023. http://dx.doi.org/10.52419/3006-2023-11-28-34.

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Glucagon-like peptide-1 is an isulin-like peptide hormone from the incretin family. The most popular pharmaceutical analogue of GLP-1 at the moment is liraglutide. GLP-1 receptors are localized in many areas of the brain responsible for the regulation of metabolic processes and eating behavior and in specific areas of the pancreas, heart, blood vessels, immune system, skin and adipose tissue, gastrointestinal tract and kidneys. We can definitely say that the effect of liraglutide extends to all tissues equipped with GLP-1 receptors, while the effect of the drug on the cardiovascular system, immune system, kidneys and gastrointestinal tract is still being studied. Also interesting is the possible effect of liraglutide on the liver, as an organ directly related to lipid and carbohydrate metabolism. In this article, we analyze the possibilities of using Saxenda, the main active ingredient of which is liraglutide, to potentiate the hepatoprotective effects of the Hepaton-vet drug in groups of rats with induced hepatopathy, evaluating the effect of these drugs on the parameters of a clinical blood test.
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Almeida, Tarcizio Souza de, Crisley Nara Bernardino Cunha, Nádia Larissa Souza Cemin, Wilma Helizabeta Horacek Melo, and Frances Tatiane Tavares Trindade. "EFEITOS DO HIPOTIREOIDISMO E SUAS MODIFICAÇÕES METABOLICAS NO ORGANISMO." In I Congresso Brasileiro de Estudos Patológicos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbesp/43.

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Introdução: O hipotireoidismo é a baixa produção de hormônios pela glândula tireoide sendo eles a tiroxina e triiodotironina responsáveis pelas funções neurológicas, cardíacas e gastrointestinais. A deficiência desses hormônios está diretamente ligada ao metabolismo onde na diminuição deles leva-se a produção de tireotrofina ou tireotrópico que atuam na regulação dos hormônios tireoidianos, porém pode provocar uma baixa metabólica. Objetivo: Conceder conhecimentos sobre o hipotireoidismo e suas mudanças fisiológicas dentro do organismo. Material e métodos: Foi abordado neste estudo de forma explicativa, uma pesquisa embasada em bibliografias e fontes de pesquisas online como por exemplo: plataforma de estudos Sanar Flix, Kenhub, Sistema Online de Busca e Análise de Literatura Médica (MEDLINE), Google Scholar (para artigos complementares), Literatura Latino-Americana e do Caribe em Ciências da Saúde (LILACS). Foram utilizados artigos selecionados usando como relevância os anos de 2010 a 2021. Resultados: O hipotireoidismo pode-se acarretar a diminuição da atividade metabólica dada a hipoatividade geral o que leva o acumulo de glicosaminoglicanos nos interstícios teciduais levando a manifestações em maioria dos sistemas do organismo, os sinais apresentados vão depender do grau e tempo da doença tendo como principais sintomas dificuldades de concentração, bradicardia, ressecamento da pele, mialgia, intolerância a frio, ganho de peso, possíveis edemas aumento da prolactina e gonadotrofina, hiporreflexia entre outros sinais. Conclusão: Portanto conclui-se que o hipotireoidismo é uma disfunção hormonal que pode acarretar inúmeros problemas por estar relacionada ao metabolismo como por exemplo a relação com o sistema cardiovascular que aumenta o risco de doenças cardíacas levando a dificuldades a práticas de exercícios físicos, com isso deve-se realizar os possíveis tratamentos sendo o principal deles a reposição hormonal.
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Hoffmann, Carlotta, Peter E. Schwarz, Christos S. Mantzoros, et al. "Circulating levels of gastrointestinal hormones in prediabetes reversing to normoglycemia or progressing to diabetes in a year – a cross-sectional and prospective analysis." In Diabetes Kongress 2023 - 57. Jahrestagung der DDG. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1767843.

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Liang, Muhua, and Xiangqian Xu. "Effect Analysis of Simotang Oral Liquid on Functional Dyspepsia of Incoordination between the Liver and the Spleen and Gastrointestinal Hormone." In 2016 7th International Conference on Mechatronics, Control and Materials (ICMCM 2016). Atlantis Press, 2016. http://dx.doi.org/10.2991/icmcm-16.2016.136.

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Sobral, Rodrigo, Janderley José De Matos, Umberto Pereira Souza Junior, and Giani Maria Cavalcante. "UTILIZAÇÃO DA CANNABIS SATIVA NO MANEJO DO ESTRESSE EM PORTADORES DE SINDROME DO INTESTINO IRRITÁVEL: UMA REVISÃO DA LITERATURA." In III Congresso Brasileiro de Ciências Farmacêuticas On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbracif/41.

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Introdução: A síndrome do intestino irritável (SII) é um distúrbio gastrointestinal crônico e remitente caracterizado por: dor abdominal, constipação ou diarreia, inchaço e flatulências. Sua fisiopatologia ainda é incompreendida, mas se dá provavelmente devido a interações complexas entre os sistemas imunológico, hormonal e nervoso. Diversos fatores são apontados como precursores, dentre eles, o estresse psicológico, que além de desestabilizar o equilíbrio e a homeostase do organismo, podem alterar as interações cérebro-intestino, afetando diferentes funções fisiológicas do sistema gastrointestinal. Muitas medidas são utilizadas para proporcionar alívio dos sintomas como o uso de medicamentos, alguns antidepressivos tricíclicos e ansiolíticos, contudo tais medidas são paliativas pois se trata de uma patologia crônica. Com o advento da ciência e a flexibilização das leis no que tangem o uso dos derivados da Cannabis sativa, muitas substâncias ativas, como por exemplo o canabidiol (CBD), são apontadas como recursos com menos efeitos colaterais e altamente eficazes nos tratamentos de diversas patologias, incluindo os distúrbios da ansiedade e estresse, sendo um importante recurso a ser considerado. Objetivo: Avaliar a eficácia da Cannabis sativa no manejo do estresse em portadores da síndrome do intestino irritável. Material e métodos: Revisão da literatura científica, apoiada em artigos indexados nas bases “Pubmed” e “Google Acadêmico”, utilizando os descritores: Estresse, Cannabis sativa, Canabidiol, Síndrome do Intestino Irritável, sendo selecionados 07 artigos originais. Como critério de inclusão, os artigos deveriam ter sido publicados entre 2016 e 2021, sendo excluído, os resumos e resumos expandidos. Resultados: A eficácia da Cannabis sativa, no manejo da SII, se dá principalmente pelos seus constituintes ativos dos quais o Canabidiol (CBD), é um de seus componentes mais estudados e com propriedades farmacológicas comprovadas frente a ansiedade e o estresse, pois tem uma afinidade com os receptor serotoninérgico 5-HT1A e o receptor CB1, e é bem conhecido que os receptores serotoninérgicos 5-HT desempenham um papel crítico na alteração relacionada ao estresse da motilidade intestinal, sensibilidade visceral e secreção intestinal, e também na fisiopatologia de distúrbios como SII. Conclusão: Por sua ação ansiolítica, é um recurso interessante no manejo do estresse e desordens emocionais, considerados fatores de agravo do quadro de SII.
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Mohammad HUSSEIN, Diyar, Khalid Hadi KADHIM, and Shaima Khazaal WAAD. "REVIEW OF THE ANATOMICAL STRUCTURES AND ROLES OF THE BIRD’S DIGESTIVE SYSTEM." In VII. INTERNATIONAL SCIENTIFIC CONGRESSOF PURE,APPLIEDANDTECHNOLOGICAL SCIENCES. Rimar Academy, 2023. http://dx.doi.org/10.47832/minarcongress7-11.

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The goal this reviews was to determined the influence of the diet on digestive system in the birds and roles of digestive tract. Birds have a very complex digestive system, which is thought to have a significant impact on how well they utilize the nutrition that they consume. It is expected that the stomach, intestines, cecum, proventriculus, and gizzard of herbivorous birds will be larger than those of carnivorous birds, whereas herbivorous birds tend to have longer, more complex digestive tracts. This may be due to herbivorous require high time and energy to the breakdown of cellulose. Their digestive processes were described for birds with different diets.. The proventriculus' size impacted by the diet, not the intestines, gizzard, or cecum. Insectivores had the largest proventriculi, whereas herbivores had the smallest, and omnivores had a proventriculus of a medium size. The function of the avian digestive organs in regulating the gut bacteria, fermenting unabsorbed nutrients, recycling nitrogen from urine, and maintaining gut health. Through aiding food uptake, and interactions with the immune system, gastrointestinal microbiota play a crucial role in maintaining organism health. Only tiny and/or soluble particles, along with digestive juices and urine, will reflux into the caeca due to anatomical and physiological adaptations. Salts and water will be reabsorbed here, and the rich bacteria will ferment uric acid and carbohydrates into ammonia and volatile fatty acids. The caeca may thereby affect the bird's nutritional health. Starch and proteins can be consumed, stored, and partially digested in the early section of the avian digestive system. With the exception of the absence of lacteals, the avian gut has a comparable anatomy to other monogastric animals. The microvilli in the avian intestine are covered by a noticeable glycocalyx. The mammalian liver's actual lobular structure is absent from the avian liver. Around the bile caniculi, hepatocytes are organized in plates two layers thick of cells. Acinar cells, that produce digesting enzymes to the pancreatic ducts, endocrine cells, that secrete hormones to the bloodstream, are found in the two main lobes and two smaller lobes of the avian pancreatic structure. The colon structure is similar to that of intestine except the poor enervation.
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Alsulami, Haneen Hamed. "INVESTIGATING THE EFFECT OF CIGARETTE SMOKING ON THE NKX3.1 AND TMPRSS2 GENES ASSOCIATED WITH MALE FERTILITY." In Dubai International Conference on Research in Life-Science & Healthcare, 22-23 February 2024. Global Research & Development Services, 2024. http://dx.doi.org/10.20319/icrlsh.2024.3041.

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Cigarette's smoking has a wide negative impact on human health, and it's have been related to many serious issues like cancer, heart disease, respiratory system, and number of health problems. Also, smoking can affect fertility in men by affecting the sperm on several levels. Our research will investigate the genetic risk factors in male by focusing on NKX3.1 and TMPRSS2 genes related to male fertility and investigate the correlation between the gene’s polymorphisms of three groups (smokers, non-smokers, and infertile men). The NKX3.1 or NK3 homeobox 1 located on chromosome 8 is the first known prostate epithelium-specific marker it is an androgen regulated transcriptional and tumor suppressor gene this gene encodes for a homeobox-containing transcription factor and the transcription factor involved in development of the testes and prostate. there are not enough research data about NKX3.1 single nucleotide’s DNA variations and interaction with cigarettes smoking. The TMPRSS2 gene or transmembrane serine protease 2 is located on chromosome 21 is an endothelial cell surface gene encodes a protein that belongs to the serine protease family. TMPRSS2 is expressed in prostate epithelial cells and is needed for normal prostate function. It’s also expressed across the gastrointestinal (digestive) tract, such as in intestinal epithelial cells and across the respiratory tract. This gives TMPRSS2 gene an advantage to study or investigate gene expression influenced by lifestyle habits such as cigarettes smoke. Most of today research is confined to respiratory and cardiovascular system affected by cigarettes smoke but this research will investigate the relation between cigarettes smoking and fertility problems in men by selecting two fertility related genes (NKX3.1 and TMPRSS2) and analyzing single nucleotide polymorphisms (SNP) From 75 blood samples collected from 25 smokers ,25 control and 25 infertile\sub-fertile men. To amplify the regions of interest within the applied gene from extracted DNA, a polymerase chain reaction (qPCR) will be used, and ELISA technique to measure serum hormones level (Testosterone and prolactin and Estrogen). We expect this research to provide new information from a new aspect about the effect of cigarettes smoking on those genes and their relation to male infertility.
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Reports on the topic "Hormones gastrointestinales"

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Yifan, Liu, and Liu Yan. Meta-analysis of two kinds of metabolic surgery for obese type 2 diabetes mellitus：A comparison of postoperative gastrointestinal hormone changes and short-term remission. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.12.0045.

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Yahav, Shlomo, John McMurtry, and Isaac Plavnik. Thermotolerance Acquisition in Broiler Chickens by Temperature Conditioning Early in Life. United States Department of Agriculture, 1998. http://dx.doi.org/10.32747/1998.7580676.bard.

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The research on thermotolerance acquisition in broiler chickens by temperature conditioning early in life was focused on the following objectives: a. To determine the optimal timing and temperature for inducing the thermotolerance, conditioning processes and to define its duration during the first week of life in the broiler chick. b. To investigate the response of skeletal muscle tissue and the gastrointestinal tract to thermal conditioning. This objective was added during the research, to understand the mechanisms related to compensatory growth. c. To evaluate the effect of early thermo conditioning on thermoregulation (heat production and heat dissipation) during 3 phases: (1) conditioning, (2) compensatory growth, (3) heat challenge. d. To investigate how induction of improved thermotolerance impacts on metabolic fuel and the hormones regulating growth and metabolism. Recent decades have seen significant development in the genetic selection of the meat-type fowl (i.e., broiler chickens); leading to rapid growth and increased feed efficiency, providing the poultry industry with heavy chickens in relatively short growth periods. Such development necessitates parallel increases in the size of visceral systems such as the cardiovascular and the respiratory ones. However, inferior development of such major systems has led to a relatively low capability to balance energy expenditure under extreme conditions. Thus, acute exposure of chickens to extreme conditions (i.e., heat spells) has resulted in major economic losses. Birds are homeotherms, and as such, they are able to maintain their body temperature within a narrow range. To sustain thermal tolerance and avoid the deleterious consequences of thermal stresses, a direct response is elicited: the rapid thermal shock response - thermal conditioning. This technique of temperature conditioning takes advantage of the immaturity of the temperature regulation mechanism in young chicks during their first week of life. Development of this mechanism involves sympathetic neural activity, integration of thermal infom1ation in the hypothalamus, and buildup of the body-to-brain temperature difference, so that the potential for thermotolerance can be incorporated into the developing thermoregulation mechanisms. Thermal conditioning is a unique management tool, which most likely involves hypothalamic them1oregulatory threshold changes that enable chickens, within certain limits, to cope with acute exposure to unexpected hot spells. Short-tem1 exposure to heat stress during the first week of life (37.5+1°C; 70-80% rh; for 24 h at 3 days of age) resulted in growth retardation followed immediately by compensatory growth" which resulted in complete compensation for the loss of weight gain, so that the conditioned chickens achieved higher body weight than that of the controls at 42 days of age. The compensatory growth was partially explained by its dramatic positive effect on the proliferation of muscle satellite cells which are necessary for further muscle hypertrophy. By its significant effect of the morphology and functioning of the gastrointestinal tract during and after using thermal conditioning. The significant effect of thermal conditioning on the chicken thermoregulation was found to be associated with a reduction in heat production and evaporative heat loss, and with an increase in sensible heat loss. It was further accompanied by changes in hormones regulating growth and metabolism These physiological responses may result from possible alterations in PO/AH gene expression patterns (14-3-3e), suggesting a more efficient mechanism to cope with heat stress. Understanding the physiological mechanisms behind thermal conditioning step us forward to elucidate the molecular mechanism behind the PO/AH response, and response of other major organs. The thermal conditioning technique is used now in many countries including Israel, South Korea, Australia, France" Ecuador, China and some places in the USA. The improvement in growth perfom1ance (50-190 g/chicken) and thermotolerance as a result of postnatal thermal conditioning, may initiate a dramatic improvement in the economy of broiler's production.
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