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2009, Número 2

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Ann Hepatol 2009; 8 (2)


Common SPINK-1 mutations do not predispose to the development of non-alcoholic fatty liver disease

Oruc N, Ozutemiz O, Salih AU, Berdeli A, Ersoz G, Gunsar F, Karasu Z, Ilter T, Batur Y
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Idioma: Ingles.
Referencias bibliográficas: 19
Paginas: 116-119
Archivo PDF: 106.70 Kb.


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REFERENCIAS (EN ESTE ARTÍCULO)

  1. Siebler J, Galle PR, Weber MM. The gut-liver-axis: endotoxemia, inflammation, insulin resistance and NASH. J Hepatol 2008; 48: 1032-4.

  2. Jiang J, Torok N. Nonalcoholic steatohepatitis and the metabolic syndrome. Metab Syndr Relat Disord 2008; 6: 1-7.

  3. El-Zayadi AR. Hepatic steatosis: A benign disease or a silent killer. World J Gastroenterol 2008; 14(26): 4120-6.

  4. Schweitz H, Vincent JP, Lazdunski M. Trypsin—pancreatic secretory inhibitor (Kazal inhibitor) interaction. Kinetic and thermodynamic properties. Biochemistry 1973; 12: 2841-6.

  5. Masamune A, Kume K, Takagi Y, Kikuta K, Satoh K, Satoh A, Shimosegawa T. N34S mutation in the SPINK1 gene is not associated with alternative splicing. Pancreas 2007; 34: 423-8.

  6. Teich N, Mössner J. Hereditary chronic pancreatitis. Best Pract Res Clin Gastroenterol 2008; 22: 115-30.

  7. Behrman SW, Fowler ES. Pathophysiology of chronic pancreatitis. Surg Clin North Am 2007; 87: 1309-24.

  8. Schneider A, Suman A, Rossi L, Barmada MM, Beglinger C, Parvin S, Sattar S, et al. SPINK1/PSTI mutations are associated with tropical pancreatitis and type II diabetes mellitus in Bangladesh. Gastroenterology 2002; 123: 1026-30.

  9. Hassan Z, Mohan V, Ali L, Allotey R, Barakat K, Faruque MO, Deepa R, et al. SPINK1 is a susceptibility gene for fibrocalculous pancreatic diabetes in subjects from the Southern Indian sub-continent. Am J Hum Genet 2002; 71: 964-8.

  10. Jönsson P, Linder C, Genell S, Ohlsson K. Extrapancreatic origin of the pancreatic secretory trypsin inhibitor as an acute-phase reactant. Pancreas 1996; 12: 303-7.

  11. Witt H, Luck W, Hennies HC, Classen M, Kage A, Lass U, Landt O, et al. Mutations in the gene encoding the serine protease inhibitor, Kazal type 1 are associated with chronic pancreatitis. Nat Genet 2000; 25: 213-6.

  12. Takamatsu S, Noguchi N, Kudoh A, Nakamura N, Kawamura T, Teramoto K, Igari T, et al. Influence of risk factors for metabolic syndrome and non-alcoholic fatty liver disease on the progression and prognosis of hepatocellular carcinoma. Hepatogastroenterology 2008; 55: 609-14.

  13. Abdelmalek MF, Liu C, Shuster J, Nelson DR, Asal NR. Familial aggregation of insulin resistance in first-degree relatives of patients with nonalcoholic fatty liver disease. Clin Gastroenterol Hepatol 2006; 4: 1162-9.

  14. Adibi A, Janghorbani M, Shayganfar S, Amini M. First-degree relatives of patients with type 2 diabetes mellitus and risk of non-alcoholic Fatty liver disease. Rev Diabet Stud 2007; 4: 236-41.

  15. Boden G. Pathogenesis of type 2 diabetes. Insulin resistance. Endocrinol Metab Clin North Am 2001; 30: 801-15.

  16. Polonsky KS, Sturis J, Bell GL. Non-insulin-dependent diabetes mellitus—a genetically programmed failure of the P cell to compensate for insulin resistance. N Engl J Med 1996; 334: 777-83.

  17. Kido H, Yokogoshi Y, Katunuma N. A low-molecular-mass Kazal-type protease inhibitor isolated from rat hepatocytes is identical to rat pancreatic secretory trypsin inhibitor II. Purification and amino acid sequence. Eur J Biochem 1990; 188: 501-6.

  18. Ohmachi Y, Murata A, Matsuura N, Yasuda T, Yasuda T, Monden M, Mori T, et al. Specific expression of the pancreatic-secretory-trypsin-inhibitor (PSTI) gene in hepatocellular carcinoma. Int J Cancer 1993; 55: 728-34.

  19. Lee YC, Pan HW, Peng SY, Lai PL, Kuo WS, Ou YH, Hsu HC. Overexpression of tumour-associated trypsin inhibitor (TATI) enhances tumour growth and is associated with portal vein invasion, early recurrence and a stage-independent prognostic factor of hepatocellular carcinoma. Eur J Cancer 2007; 43: 736-44.




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Ann Hepatol. 2009;8

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