Gastrointestinal Hormones and Receptors

Miller, Laurence J.

doi:10.1002/9781118512074.ch13

Cited by 3 publications

(6 citation statements)

References 219 publications

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“…Our results related to amylin, GLP-1, and glucagon are consistent with previous studies, and the known physiologic effects of these hormones, specifically that increased levels, are associated with limited EN delivery. 2,9,15 The relationship between ghrelin and PYY and gastric emptying by C1h differs from previous studies and may represent a unique physiologic response in critically ill children or may be secondary to different study conditions between our study and prior studies. 13,14,16 EN tolerance and gastric emptying are influenced by multiple factors, and our results support gastrointestinal hormone changes as one of these contributing factors.…”

Section: Discussioncontrasting

confidence: 76%

“…The role of gastrointestinal hormones on gastrointestinal physiology in healthy subjects has been extensively studied. [8][9][10][11][12] In summary, CCK, PYY, GLP-1, amylin, and GIP delay gastric emptying primarily during fed states, whereas ghrelin stimulates gastric emptying and glucagon delays gastric emptying in fasting states. [9][10][11][12] Critical illness can influence gastrointestinal hormone levels, resulting in different gastrointestinal pathophysiologic effects.…”

Section: Discussionmentioning

confidence: 99%

“…Gastrointestinal hormones orchestrate gastric emptying and whole gastrointestinal motility, which are essential for optimal nutrient digestion and absorption. [8][9][10][11][12] Levels of multiple gastrointestinal hormones have been explored in relation to gastric emptying and EN intolerance in critically ill adults. [13][14][15][16][17] For example, cholecystokinin (CCK) and peptide-YY (PYY) have been reported to be elevated in critically ill adults with delayed gastric emptying.…”

Section: Introductionmentioning

confidence: 99%

“…Gastrointestinal hormones orchestrate gastric emptying and whole gastrointestinal motility, which are essential for optimal nutrient digestion and absorption . Levels of multiple gastrointestinal hormones have been explored in relation to gastric emptying and EN intolerance in critically ill adults .…”

Section: Introductionmentioning

confidence: 99%

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Gastrointestinal Hormone Profiles Associated With Enteral Nutrition Tolerance and Gastric Emptying in Pediatric Critical Illness: A Pilot Study

Martinez

Panciotti

Pereira

et al. 2019

J Parenter Enteral Nutr

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Background Enteral nutrition (EN) intolerance and delayed gastric emptying are prevalent in pediatric critical illness and limit EN delivery. Gastrointestinal (GI) hormones may be associated with EN intolerance and delayed gastric emptying in this cohort. Methods We determined GI hormone levels, time to achieve 50% of EN goal, and gastric emptying in critically ill children. Total amylin, active ghrelin, total glucagon‐like peptide‐1 (GLP‐1), total gastric inhibitory polypeptide, glucagon, and total peptide‐YY (PYY) were measured by multiplex assay and cholecystokinin by ELISA. Lower concentrations of acetaminophen at 1 hour (C1h, µg/mL) using the acetaminophen absorption test defined delayed gastric emptying. Correlation, regression analyses, and a principal component analysis were used to examine the association between GI hormones and time to 50% EN goal and C1h. Results GI hormones were measured in 14 of 21 patients with gastric emptying testing; median age of 11.2 years (6.74–16.3) and 50% male. Increasing hormone levels from GI hormone profile 1 (GLP‐1, glucagon, and amylin) correlated with greater time to reach 50% EN goal (R2 = 0.296, P = 0.04). Decreasing hormone levels from GI hormone profile 2 (PYY and ghrelin) correlated with lower C1h and slower gastric emptying (R2 = 0.342, P = 0.02). Conclusion GI hormone profiles are associated with time to achieve 50% of EN goal and gastric emptying in critically ill children. We have described a feasible model to study the role of GI hormones in this cohort, including the potential clinical applicability of GI hormone measurement in the management of delayed gastric emptying.

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Section: Discussioncontrasting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Gastrointestinal Hormone Profiles Associated With Enteral Nutrition Tolerance and Gastric Emptying in Pediatric Critical Illness: A Pilot Study

Martinez

Panciotti

Pereira

et al. 2019

J Parenter Enteral Nutr

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“…The GI tract produces and releases enzymes and peptide hormones, including gastrin, secretin, cholecystokinin, gastric inhibitory peptide (GIP), and motilin in order to help the digestive process, as well as local factors such as prostaglandins, histamine, and other molecules, released into the interstitial fluid. These molecules coordinate the response to local pH variation, presence of chemical substances, or physical stimuli [1][2][3][4][5][6][7]. When homeostasis is challenged by pathogen or injury, inflammation occurs and the GI tract switches the balance from an absorptive state to a secretory status [5,6].…”

Section: Introductionmentioning

confidence: 99%

Gut–Brain Axis: Focus on Neurodegeneration and Mast Cells

2020

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Many studies highlighted that a bidirectional communication between the gut and the central nervous system (CNS) exists. A vigorous immune response to antigens must be avoided, and pathogenic organisms crossing the gut barrier must be detected and killed. For this reason, the immune system developed fine mechanisms able to maintain this delicate balance. The microbiota is beneficial to its host, providing protection against pathogenic bacteria. It is intimately involved in numerous aspects of host physiology, from nutritional status to behavior and stress response. In the last few years, the implication of the gut microbiota and its bioactive microbiota-derived molecules in the progression of multiple diseases, as well as in the development of neurodegenerative disorders, gained increasing attention. The purpose of this review is to provide an overview of the gut microbiota with particular attention toward neurological disorders and mast cells. Relevant roles are played by the mast cells in neuroimmune communication, such as sensors and effectors of cytokines and neurotransmitters. In this context, the intake of beneficial bacterial strains as probiotics could represent a valuable therapeutic approach to adopt in combination with classical therapies. Further studies need to be performed to understand if the gut bacteria are responsible for neurological disorders or if neurological disorders influence the bacterial profile.

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Parameters of blood short-chain peptides and digestive hydrolases in patients with chronic hepatitis B virus infection

Жураева

Алейник

Ashuralieva

et al. 2021

Russian Journal of Infection and Immunity

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The aim of the study was to examine specifics of changes in the level of stomach- and pancreas-released blood hydrolases in chronic viral hepatitis B and analyze the mechanisms underlying such changes. We assessed serum markers of HBV infection, liver enzymes tests as well as gastric and pancreatic hydrolase level. The patients examined were divided into three groups: control (healthy) and two study groups — HBV post-infection and chronic HBV infection. Patients with HBV post-infection had no significant deviations from normal range for blood level of gastric and pancreatic hydrolases. Patients with chronic HBV infection were found to contain increased blood level of amylase and lipase, which may evidence about increasing pancreatic functional activity and development of covert pancreatitis. At the same time, decline in the concentration of serum pepsinogen-1 below 40 μg/l could indicate about prominently decreased secretion of hydrochloric acid and development of atrophic gastritis, and it was found that the major factor contributing to development of such disorders was the short-chain peptide CCK-8, which utilization declines in patients with chronic HBV infection. CCK-8 can play a pivotal role in inhibiting stimulation of gastric acid secretion and controls gastric acid, plasma gastrin and somatostatin secretion. Cholecystokinin has been found to inhibit acid secretion by activating CCK type A receptors as well as via somatostatin-involving mechanism. The secretion of gastric somatostatin-14 increased by fivefold due to CCK-8 alone, but was blocked by the CCK-A receptor blocker loxiglumide. These data show that CCK-8 directly inhibits acid reactions by stimulating the release of gastric somatostatin indirectly through the CCK-A receptor. Thus, it can be assumed that normally CCK-8 is mainly utilized by the liver, which is altered during chronic hepatitis B resulting in elevated blood CCK-8 concentration. As a consequence, it enhances pancreatic secretion resulting in developing pancreatitis that is paralleled with inhibited gastric secretion and emerged atrophic gastritis.

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Gastrointestinal Hormones and Receptors

Cited by 3 publications

References 219 publications

Gastrointestinal Hormone Profiles Associated With Enteral Nutrition Tolerance and Gastric Emptying in Pediatric Critical Illness: A Pilot Study

Gastrointestinal Hormone Profiles Associated With Enteral Nutrition Tolerance and Gastric Emptying in Pediatric Critical Illness: A Pilot Study

Gut–Brain Axis: Focus on Neurodegeneration and Mast Cells

Parameters of blood short-chain peptides and digestive hydrolases in patients with chronic hepatitis B virus infection

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