Next Article in Journal
Effects of Pharmacological Thermogenic Adipocyte Activation on Metabolism and Atherosclerotic Plaque Regression
Next Article in Special Issue
Pterostilbene Reduces Liver Steatosis and Modifies Hepatic Fatty Acid Profile in Obese Rats
Previous Article in Journal
Congenital Lactase Deficiency: Mutations, Functional and Biochemical Implications, and Future Perspectives
Previous Article in Special Issue
Eucommia ulmoides Leaf Extract Ameliorates Steatosis Induced by High-fat Diet in Rats by Increasing Lysosomal Function
Open AccessReview

The Relevance of Toxic AGEs (TAGE) Cytotoxicity to NASH Pathogenesis: A Mini-Review

1
Department of Advanced Medicine, Medical Research Institute, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0293, Japan
2
Department of Biochemistry, Faculty of Pharmaceutical Sciences, Hiroshima International University, 5-1-1, Hirokoshingai, Kure, Hiroshima 737-0112, Japan
*
Author to whom correspondence should be addressed.
Nutrients 2019, 11(2), 462; https://doi.org/10.3390/nu11020462
Received: 31 January 2019 / Revised: 18 February 2019 / Accepted: 18 February 2019 / Published: 22 February 2019
Non-alcoholic fatty liver disease (NAFLD) is currently the most common feature of chronic liver disease. Non-alcoholic steatohepatitis (NASH) is a severe form of NAFLD, and one of its risk factors is hyperglycemia. The chronic ingestion of excessive amounts of high-fructose corn syrup is associated with an increased prevalence of fatty liver. Under hyperglycemic conditions, advanced glycation end-products (AGEs) are generated through a non-enzymatic glycation reaction between the ketone or aldehyde groups of sugars and amino groups of proteins. Glyceraldehyde (GA) is a metabolic intermediate of sugars, and GA-derived AGEs (known as toxic AGEs (TAGE)) have been implicated in the development of NASH. TAGE accumulates more in serum or liver tissue in NASH patients than in healthy controls or patients with simple steatosis. Furthermore, the TAGE precursor, GA, causes cell damage through protein dysfunctions by TAGE modifications and induces necrotic-type hepatocyte death. Intracellular TAGE may leak outside of necrotic-type cells. Extracellular TAGE then induce inflammatory or fibrotic responses related to the pathology of NASH in surrounding cells, including hepatocytes and hepatic stellate cells. This review focuses on the contribution of TAGE to the pathology of NASH, particularly hepatic cell death related to NASH. View Full-Text
Keywords: non-alcoholic fatty liver disease (NAFLD); non-alcoholic steatohepatitis (NASH); advanced glycation end-products (AGEs); glyceraldehyde (GA); glyceraldehyde-derived AGEs; toxic AGEs (TAGE); hepatocytes; hepatocyte stellate cell (HSCs) non-alcoholic fatty liver disease (NAFLD); non-alcoholic steatohepatitis (NASH); advanced glycation end-products (AGEs); glyceraldehyde (GA); glyceraldehyde-derived AGEs; toxic AGEs (TAGE); hepatocytes; hepatocyte stellate cell (HSCs)
Show Figures

Figure 1

MDPI and ACS Style

Sakasai-Sakai, A.; Takata, T.; Takino, J.-I.; Takeuchi, M. The Relevance of Toxic AGEs (TAGE) Cytotoxicity to NASH Pathogenesis: A Mini-Review. Nutrients 2019, 11, 462.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop