Ghrelin and gastroparesis as early predictors of clinical outcomes in acute pancreatitis

Wu, Landy M.; Premkumar, Rakesh; Phillips, Anthony R.J.; Windsor, John A.; Petrov, Maxim S.

doi:10.1016/j.pan.2015.12.002

Cited by 14 publications

(8 citation statements)

References 63 publications

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“…In particular, ghrelin is also secreted in the pancreas. 51 , 52 Fifth, we assumed that the different circulating level of the peptides investigated in this study reflect their level of secretion while, in theory, it might also be attributed to a differential inactivation of the peptides by corresponding exopeptidases. 53 However, with the exception of dipeptidyl peptidase-4 for GLP-1 (which was not significantly changed in this study), there is no commercially available assay to measure them.…”

Section: Discussionmentioning

confidence: 97%

The Role of Gut–brain Axis in Regulating Glucose Metabolism After Acute Pancreatitis

Pendharkar

Asrani

Murphy

et al. 2017

Clinical and Translational Gastroenterology

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Objectives:Diabetes has become an epidemic in developed and developing countries alike, with an increased demand for new efficacious treatments. A large body of pre-clinical evidence suggests that the gut–brain axis may be exploited as a potential therapeutic target for defective glucose homeostasis. This clinical study aimed to investigate a comprehensive panel of glucoregulatory peptides, released by both the gut and brain, in individuals after acute pancreatitis.Methods:Fasting levels of glucagon-like peptide-1 (GLP-1), glicentin, oxyntomodulin, peptide YY, ghrelin, cholecystokinin, vasoactive intestinal peptide (VIP), and secretin were studied. Modified Poisson and multivariable linear regression analyses were conducted. Pre-determined concentration ranges were used to categorize each peptide into quartiles.Results:A total of 83 individuals were included, of who 30 (36%) developed abnormal glucose metabolism (AGM) after acute pancreatitis. In individuals with AGM, the highest quartile of oxyntomodulin differed most significantly from the lowest quartile with a prevalence ratio (PR; 95% confidence interval) of 0.50 (0.21, 1.20; P=0.005); of glicentin with a PR of 0.26 (0.13, 0.54; P<0.001); and of VIP with a PR of 0.34 (0.13, 0.89; P=0.043). Peptide YY, GLP-1, cholecystokinin, ghrelin, and secretin were not significantly associated with AGM.Conclusions:Fasting circulating oxyntomodulin, glicentin, and VIP levels are significantly decreased in patients with defective glucose homeostasis after acute pancreatitis. Oxyntomodulin appears to be a promising therapeutic target for future clinical studies on diabetes associated with diseases of the exocrine pancreas.

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Section: Discussionmentioning

confidence: 97%

The Role of Gut–brain Axis in Regulating Glucose Metabolism After Acute Pancreatitis

Pendharkar

Asrani

Murphy

et al. 2017

Clinical and Translational Gastroenterology

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“…Moreover, the GCSI responded well to clinical change, as evidenced by strong total score reduction over the study period in the entire cohort and by significantly better appetite in those patients who received enteral feeding. A subsequent pilot clinical study by COSMOS group found that the GCSI can be used as an early predictor of feeding intolerance as well as non-mild course of acute pancreatitis [5]. This was followed by a prospective cohort study of 217 patients with acute pancreatitis (also conducted by COSMOS group), which confirmed clinical usefulness of the GCSI in prediction of feeding intolerance [6].…”

Section: Editorialmentioning

confidence: 80%

The nescience and nascence of gastrointestinal motility research in acute pancreatitis

Petrov

2017

Scandinavian Journal of Gastroenterology

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“…In clinical studies, the ghrelin serum level was not found to be a predictor of the severity of disease; however, its combination with the Gastroparesis Cardinal Symptom Index improved its predictive accuracy (34,35). other studies reported that ghrelin could be implicated in the natural protection of the pancreatic tissue through the activation of the innate immune system to prevent the development of the inflammatory process in the pancreas.…”

Section: Discussionmentioning

confidence: 99%

Cav 1.2 and Cav 2.2 expression is regulated by different endogenous ghrelin levels in pancreatic acinar cells during acute pancreatitis

et al. 2018

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Ghrelin influences pancreatic endocrine and exocrine functions, regulates intracellular calcium [Ca2+]i levels, and has an anti-inflammatory role in acute pancreatitis. This study investigated the role of endogenous ghrelin in the expression of Cav 1.2 (L-type of Ca2+ channel) and Cav 2.2 (N-type of Ca2+ channel) in acute pancreatitis. For this purpose, acute edematous pancreatitis (AEP) and acute necrotizing pancreatitis (ANP) rat models were established. Cav 1.2 and Cav 2.2 expression was assessed by immunohistochemistry in the pancreatic tissues of rats; ghrelin, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) serum levels were detected using ELISA. Next, in AR42J cells with either knock-out or overexpression of ghrelin, Cav 1.2 and Cav 2.2 expression was examined using western blot analysis, and intracellular calcium [Ca2+]i was detected with confocal microscopy. In this study, the ghrelin serum level was highest in the ANP group and was higher in the AEP group than the normal group. Expression of Cav 1.2 and Cav 2.2 in the ANP and AEP groups was higher than in the respective control groups. The serum IL-1β and TNF-α levels were significantly higher in the ANP group compared to the other groups. Cav 1.2 and Cav 2.2 expression and [Ca2+]i decreased in ghrelin knockdown AR42J cells but increased in ghrelin overexpressing cells. In conclusion, Cav 1.2 and Cav 2.2 expression increased in ANP. The [Ca2+]i level, which is mediated by Cav 1.2 and Cav 2.2 expression, is directly regulated by ghrelin in pancreatic acinar cells, and serum ghrelin levels may be involved in the severity of acute pancreatitis.

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Ghrelin and gastroparesis as early predictors of clinical outcomes in acute pancreatitis

Cited by 14 publications

References 63 publications

The Role of Gut–brain Axis in Regulating Glucose Metabolism After Acute Pancreatitis

The Role of Gut–brain Axis in Regulating Glucose Metabolism After Acute Pancreatitis

The nescience and nascence of gastrointestinal motility research in acute pancreatitis

Cav 1.2 and Cav 2.2 expression is regulated by different endogenous ghrelin levels in pancreatic acinar cells during acute pancreatitis

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