Role of Ghrelin in the Pathophysiology of Gastrointestinal Disease

Cheung, CL; Wu, Justin Che Yuen

doi:10.5009/gnl.2013.7.5.505

Cited by 52 publications

(49 citation statements)

References 82 publications

(98 reference statements)

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“…A study by Cheung and Wu [6] supports the hypothesis that abnormal ghrelin responses may play an important role in various GI disorders. Similarly, Kazemi et al [7] demonstrated that significantly different ghrelin levels in dyspeptic patients and healthy controls may play an important role in the induction of symptoms in functional dyspepsia (FD) patients.…”

Section: Introductionmentioning

confidence: 63%

“…Furthermore, human clinical trials and animal studies involving the administration of ghrelin or its receptor agonists have shown promising improvements in delayed gastric emptying [6]. Besides, along with blocking leptin activity, the correlations among leptin-mediated cellular immune response, systemic leptin levels, and amount of adipose tissues may provide new strategies for therapeutic intervention in autoimmune diseases, especially for intestinal inflammation [10].…”

Section: Introductionmentioning

confidence: 99%

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Gastroduodenal Symptoms in Inflammatory Bowel Disease Are Correlated with Gastric Emptying and Serum Levels of Active Ghrelin

Sales

Cavalcanti

Souza

et al. 2019

Dig Dis

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Background: Inflammatory bowel disease (IBD) is associated with delay in gastric emptying, increase in ghrelin, and decrease in leptin. The aim was to investigate the correlation between gastroduodenal (GD) symptoms, gastric emptying, and serum levels of active ghrelin and leptin in IBD. Twenty-seven IBD patients and 26 healthy volunteers were asked to complete the Porto Alegre Dyspeptic Symptoms Questionnaire. A gastric emptying test for solids was performed using a C13 octanoic acid breath test. During this test, serum samples were collected for measuring active ghrelin and leptin concentrations by radioimmunoassay. Summary: Patients with IBD demonstrated delayed gastric emptying compared with healthy volunteers. In patients with GD symptoms, the delay in gastric emptying was more pronounced, and there were significant correlations of satiety and vomiting with gastric emptying. Basal leptin, but not active ghrelin, increased in patients with GD symptoms compared with patients without these symptoms. There were negative correlations between basal active ghrelin with total Porto Alegre score and epigastric pain in IBD patients with GD symptoms. Key Messages: In IBD, satiety and vomiting were associated with delay in gastric emptying. Conversely, epigastric pain had a negative correlation with active ghrelin. Our results suggest that different pathophysiological mechanisms contribute to GD symptoms in IBD.

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Section: Introductionmentioning

confidence: 63%

Section: Introductionmentioning

confidence: 99%

Gastroduodenal Symptoms in Inflammatory Bowel Disease Are Correlated with Gastric Emptying and Serum Levels of Active Ghrelin

Sales

Cavalcanti

Souza

et al. 2019

Dig Dis

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“…The functions of ghrelin include food intake regulation, gastrointestinal (GI) motility, and acid secretion in the GI tract. Many GI disorders involving infection, inflammation, and malignancy are correlated with altered ghrelin production and secretion [98] .…”

Section: Ghrelinmentioning

confidence: 99%

Cancer cachexia, mechanism and treatment

Aoyagi¹,

Terracina²,

Ali³

et al. 2015

WJGO

346

261

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It is estimated that half of all patients with cancer eventually develop a syndrome of cachexia, with anorexia and a progressive loss of adipose tissue and skeletal muscle mass. Cancer cachexia is characterized by systemic inflammation, negative protein and energy balance, and an involuntary loss of lean body mass. It is an insidious syndrome that not only has a dramatic impact on patient quality of life, but also is associated with poor responses to chemotherapy and decreased survival. Cachexia is still largely an underestimated and untreated condition, despite the fact that multiple mechanisms are reported to be involved in its development, with a number of cytokines postulated to play a role in the etiology of the persistent catabolic state. Existing therapies for cachexia, including orexigenic appetite stimulants, focus on palliation of symptoms and reduction of the distress of patients and families rather than prolongation of life. Recent therapies for the cachectic syndrome involve a multidisciplinary approach. Combination therapy with diet modification and/or exercise has been added to novel pharmaceutical agents, such as Megestrol acetate, medroxyprogesterone, ghrelin, omega-3-fatty acid among others. These agents are reported to have improved survival rates as well as quality of life. In this review, we will discuss the emerging understanding of the mechanisms of cancer cachexia, the current treatment options including multidisciplinary combination therapies, as well an update on new and ongoing clinical trials.

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“…hormone (5). It is secreted primarily by endocrine cells of the oxyntic glands of the gastric fundus and to a lesser extent by the body of the stomach, the mucosa of the duodenum and jejunum, the lungs, the urogenital organs, and the pituitary gland.…”

mentioning

confidence: 99%

“…Ghrelin is a well-known orexigenic hormone that stimulates food intake in a dose-dependent manner (5)(6)(7)(8). Ghrelin increases appetite both by initiating homeostatic feeding driven by metabolic need and by non-homeostatic feeding, acting centrally and affecting the modulation of reward, memory and motivated feeding behavior (9).…”

mentioning

confidence: 99%

Ghrelin and Obesity: Identifying Gaps and Dispelling Myths. A Reappraisal

Makris

Alexandrou

Papatsoutsos

et al. 2017

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Abstract. The etiology of obesity is complex. Environmental and genetic causes have been implicated in the development of this disease. Ghrelin is a hormoneObesity is a major public health problem as more than 10% of the global population is obese (1). The number of patients affected by this modern epidemic and the associated comorbidities, such as diabetes mellitus, cardiovascular diseases and cancer, are constantly rising, along with the associated health costs, making the management of obesity one of paramount importance (2, 3).There are mainly two ways to manage obesity: the conservative one (e.g. diet, exercise and lifestyle changes) and the surgical approach through various weight-loss surgical procedures, widely known as bariatric surgery.Surgery not only leads to malabsorption (calories are not taken up by the intestine), mechanical restriction (less room for food), but also to hormonal changes that lead to less hunger or earlier satiety postprandially (3, 4).During the past couple of decades the identification of circulating factors that contribute to the induction of hunger (orexigenic) or satiety (anorexigenic) has diversified the cause of food restriction after bariatric surgery apart from being solely a mechanical phenomenon to a more complex effect of both anatomical and humoral modifications induced by the different operative strategies.Ghrelin is a well-known orexigenic hormone that stimulates food intake in a dose-dependent manner (5-8). Ghrelin increases appetite both by initiating homeostatic feeding driven by metabolic need and by non-homeostatic feeding, acting centrally and affecting the modulation of reward, memory and motivated feeding behavior (9).In this review, we planned to highlight the available data regarding the appetite-generating effect of ghrelin. We searched the literature in order to find determinants with a proven direct positive feedback in appetite.

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Role of Ghrelin in the Pathophysiology of Gastrointestinal Disease

Cited by 52 publications

References 82 publications

Gastroduodenal Symptoms in Inflammatory Bowel Disease Are Correlated with Gastric Emptying and Serum Levels of Active Ghrelin

Gastroduodenal Symptoms in Inflammatory Bowel Disease Are Correlated with Gastric Emptying and Serum Levels of Active Ghrelin

Cancer cachexia, mechanism and treatment

Ghrelin and Obesity: Identifying Gaps and Dispelling Myths. A Reappraisal

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