Endogenous formation of Nε-(carboxymethyl)lysine is increased in fatty livers and induces inflammatory markers in an in vitro model of hepatic steatosis.

@article{Gaens2012EndogenousFO,
  title={Endogenous formation of N$\epsilon$-(carboxymethyl)lysine is increased in fatty livers and induces inflammatory markers in an in vitro model of hepatic steatosis.},
  author={Katrien H.J. Gaens and Petra M. G. Niessen and Sander S. Rensen and Wim A. Buurman and Jan Willem M. Greve and Ann Driessen and Marcel G. M. Wolfs and Marten H. Hofker and Johanne G. Bloemen and Cornelis H C Dejong and Coen D. A. Stehouwer and Casper G. Schalkwijk},
  journal={Journal of hepatology},
  year={2012},
  volume={56 3},
  pages={
          647-55
        }
}

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References

SHOWING 1-10 OF 35 REFERENCES
The Nε-(carboxymethyl)lysine–RAGE axis: putative implications for the pathogenesis of obesity-related complications
TLDR
The putative role of CML-modified proteins in obesity is addressed and the identification of this pathway may provide an important strategy for novel therapeutic approaches against obesity-associated complications.
Advanced glycation end products enhance the proliferation and activation of hepatic stellate cells
TLDR
Data indicate that AGEs induce ROS generation and intensify the proliferation and activation of HSCs, supporting the possibility that antioxidants may represent a promising treatment for prevention of the development of hepatic fibrosis in NASH.
Increased hepatic myeloperoxidase activity in obese subjects with nonalcoholic steatohepatitis.
TLDR
Accumulation of MPO-mediated oxidation products, partly derived from Kupffer cell MPO, is associated with induction of CXC chemokines and hepatic neutrophil infiltration and may contribute to the development of NASH.
Atorvastatin decreases serum levels of advanced glycation endproducts (AGEs) in nonalcoholic steatohepatitis (NASH) patients with dyslipidemia: clinical usefulness of AGEs as a biomarker for the attenuation of NASH
TLDR
It is demonstrated that atorvastatin decreased the serum levels of AGEs in NASH patients with dyslipidemia and suggested the usefulness of A GEs as a biomarker for the attenuation of NASH is suggested.
The AGE inhibitor pyridoxamine inhibits lipemia and development of renal and vascular disease in Zucker obese rats.
TLDR
Lipids are an important source of chemical modification of tissue proteins, even in the absence of hyperglycemia and pyridoxamine inhibited AGE/ALE formation and hyperlipidemia and protected against renal and vascular pathology in a nondiabetic model.
Systemic Markers of Lipid Peroxidation and Antioxidants in Patients with Nonalcoholic Fatty Liver Disease
TLDR
The results concerning correlations suggest that disturbances in BMI, body fat, and lipid metabolism may contribute to altered oxidative status in NAFLD, and insulin resistance may be related to decreased antioxidants inNAFLD as well as products of lipid peroxidation.
...
...