Journals / Turkish Journal of Gastroenterology / 2014 / Cilt: 25 - Sayı: 6

New hormones to predict the severity of gallstone-induced acute pancreatitis

Pages
714–717
DOI
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

To clarify whether the magnitude of the change in hormone levels at AP onset can be used as a biomarkers to predict the severity of the disease requires further investigation.

📌 3 Key Takeaways

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Objective & Hypothesis:Background/Aims: Levels of the hormones ghrelin and leptin in rat models of acute pancreatitis (AP) have been investigated in several experimental studies.
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Key Findings & Data:A few recent studies investigating the changes in ghrelin and leptin levels in patients with AP have been reported; however, our study is the first clinical study to investigate the change of nesfatin-1 levels in patients with gallstone-induced AP.Materials and Methods: Forty patients were enrolled in this study, eight of which presented with severe AP.
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Conclusion & Impact:To clarify whether the magnitude of the change in hormone levels at AP onset can be used as a biomarkers to predict the severity of the disease requires further investigation.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Background/Aims: Levels of the hormones ghrelin and leptin in rat models of acute pancreatitis (AP) have been investigated in several experimental studies. However, there are very few clinical studies addressing the connection between hormone levels and AP. A few recent studies investigating the changes in ghrelin and leptin levels in patients with AP have been reported; however, our study is the first clinical study to investigate the change of nesfatin-1 levels in patients with gallstone-induced AP.Materials and Methods: Forty patients were enrolled in this study, eight of which presented with severe AP. Two blood samples were obtained from each study patient. The first blood samples were obtained at patient admission to the hospital and the second was obtained at patient discharge. All samples were collected after at least 6 h of fasting. Plasma nesfatin-1, leptin, and ghrelin levels were measured. Results: In all 40 patients, nesfatin-1 and leptin levels were higher at admission and had decreased at discharge. In contrast, the ghrelin levels at discharge were significantly higher than those at admission. Only the changes in these hormones in the mild AP group were significant. Conclusion: Levels of these hormones were altered during the course of gallstone-induced AP. These changes might be associated with the clinical outcomes of the disease. To clarify whether the magnitude of the change in hormone levels at AP onset can be used as a biomarkers to predict the severity of the disease requires further investigation.

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Cite This Article

ÜLGER, B. V., GÜL, M., USLUKAYA, Ö., OĞUZ, A., BOZDAĞ, Z., YÜKSEL, H., BÖYÜK, A. (2014). New hormones to predict the severity of gallstone-induced acute pancreatitis. Turkish Journal of Gastroenterology, Cilt: 25 - Sayı: 6, 714–717. https://ajindex.com/articles/411088

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References (16)

  1. Fisher WE, Brunicardi FC, Bell RH, Andersen DK, Saluja AK. Pancreas. In: Brunicardi FC. Schwartz's Principles of Surgery. New York: The McGraw-Hill Company; 2010.p.2240-381
  2. Gardner TB, Berk BS. Acute Pancreatitis. Medscape Available from: http://emedicine.medscape.com/article/181364-overview. 2010
  3. Nagar AB, Gorelick FS. Epidemiology and pathophysiology of acute pancreatitis. In: Forsmark CE. Pancreatitis and its Complications. Totawa, NJ: Humana Press; 2010.p.3-16
  4. Khanna AK, Meher S, Prakash S, et al. Comparison of Ranson, Glasgow, MOSS, SIRS, BISAP, APACHE-II, CTSI Scores, IL-6, CRP, and Procalcitonin in Predicting Severity, Organ Failure, Pancreatic Necrosis, and Mortality in Acute Pancreatitis. HPB Surg 2013; 2013: 367581
  5. Oh-I S, Shimuzu H, Satoh T, et al. Identification of nesfatin-1 as a satiety molecule in the hypothalamus. Nature 2006; 443: 709-12
  6. Gonzalez R, Tiwari A, Unniappan S. Pancreatic beta cells colocalize insulin and pronesfatin immunoreactivity in rodents. Biochem Biophys Res Commun 2009; 381: 643-8
  7. Foo KS, Brauner H, Ostenson C-G, Broberger C. Nucleobindin-2/ nesfatin in the endocrine pancreas: distribution and relationship to glycaemic state. J Endocrinol 2010; 204: 255-63
  8. Shimizu, Oh-I S, Hashimoto K, et al. Peripheral administration of nesfatin-1 reduces food intake in mice: the leptin-independent mechanism endocrinology. Endocrinology 150: 662-71
  9. Su Y, Zhang J, Tang Y, Bi F, Liu JN. The novel function of nesfatin-1: Anti-hyperglycemia. Biochem Biophys Res Commun 2010; 391: 1039-42
  10. Stengel A, Goebel M, Wang L, et al. Central nesfatin-1 reduces dark-phase food intake and gastric emptying in rats: differential role of corticotropin-releasing factor2 receptor; Endocrinology 2009; 150: 4911-19
  11. Arnes L, Hill JT, Gross S, Magnuson MA, Sussel L. Ghrelin expression in the mouse pancreas defines a unique multipotent progenitor population; PLoS One 2012; 7: e52026
  12. Kerem M, Bedirli A, Pasaoglu H, et al. Role of ghrelin and leptin in predicting the severity of acute pancreatitis. Dig Dis Sci 2007; 52: 950-5
  13. Fujitsuka N, Asakawa A, Amitani H, Fujimiya M, Inui A. Ghrelin and gastrointestinal movement; Methods Enzymol 2012; 514: 289- 301
  14. Zhang W, Chen M, Chen X, et al. Inhibition of pancreatic protein secretion by ghrelin in the rat. J Physiol 2001; 537: 231-6
  15. Marwarha G, Ghribi O. Leptin signaling and Alzheimer's disease; Am J Neurodegener Dis 2012; 1: 245-65
  16. Kiefer TJ, Heller RS,