Display options
Cite
Pár A, Pár G. Újabb adatok a nem alkoholos zsírmáj patogeneziséhez. [Advances in the pathogenesis of non alcoholic fatty liver disease]. Orv Hetil. 2017;158(23):882-894doi: 10.1556/650.2017.30775.
Pár, A., & Pár, G. (2017). Újabb adatok a nem alkoholos zsírmáj patogeneziséhez. [Advances in the pathogenesis of non alcoholic fatty liver disease]. Orvosi hetilap, 158(23), 882-894. https://doi.org/10.1556/650.2017.30775
Pár, Alajos, and Pár, Gabriella. "Újabb adatok a nem alkoholos zsírmáj patogeneziséhez." [Advances in the pathogenesis of non alcoholic fatty liver disease]. Orvosi hetilap vol. 158,23 (2017): 882-894. doi: https://doi.org/10.1556/650.2017.30775
Pár A, Pár G. Újabb adatok a nem alkoholos zsírmáj patogeneziséhez. [Advances in the pathogenesis of non alcoholic fatty liver disease]. Orv Hetil. 2017 Jun;158(23):882-894. doi: 10.1556/650.2017.30775. Hungarian. PMID: 28580850.
Copy Download .nbib Format: NLM
Share it on

Orv Hetil. 2017 Jun;158(23):882-894. doi: 10.1556/650.2017.30775.

[Advances in the pathogenesis of non alcoholic fatty liver disease].

Orvosi hetilap

[Article in Hungarian]
Alajos Pár, Gabriella Pár

Affiliations

  1. Klinikai Központ, I. Belgyógyászati Klinika, Pécsi Tudományegyetem, Általános Orvostudományi Kar Pécs, Ifjúság u. 13., 7624.

PMID: 28580850 DOI: 10.1556/650.2017.30775

Abstract

Non alcoholic fatty liver disease is the hepatic manifestation of metabolic syndrome, and the most common liver disease. Its more aggressive form is the non alcoholic steatohepatitis. Multiple genetic and environmental factors lead to the accumulation of triglicerides and the inflammatory cascade. High fat diet, obesity, adipocyte dysfunction with cytokine production, insulin resistance and increased lipolysis with free fatty acid flux into the liver - all are the drivers of liver cell injury. Activation of inflammasome by damage- or pathogen-associated molecular patterns results in "steril inflammation" and immune response, while the hepatic stellate cells and progenitor cells lead to fibrogenesis. Small intestinal bacterial overgrowth and gut dysbiosis are also of pivotal importance in the inflammation. Among the susceptible genetic factors, mutations of patatin-like phospholipase domain containing 3 and the transmembrane 6 superfamily 2 genes play a role in the development and progression of the disease, similarly as do epigenetic regulators such as microRNAs and extracellular vesicles. Better understanding of the pathogenesis of non alcoholic fatty liver disease may identify novel therapeutic agents that improve the outcome of the disease. Orv Hetil. 2017; 158(23): 882-894.

Keywords: nem alkoholos steatohepatitis; nem alkoholos zsírmáj; non alcoholic fatty liver disease; non alcoholic steatohepatitis; pathogenesis; patogenezis

MeSH terms

Publication Types