Oltipraz for Liver Fat Reduction in Patients With Non-alcoholic Fatty Liver Disease Except for Liver Cirrhosis

  • STATUS
    Recruiting
  • days left to enroll
    87
  • participants needed
    144
  • sponsor
    PharmaKing
Updated on 25 January 2021
Investigator
Min-Goo Yang, Director
Primary Contact
Wonju Severance Christian Hospital (7.5 mi away) Contact
+14 other location
body mass index
liver disease
cirrhosis
fatty acids
neutrophil count
fatty liver

Summary

Oltipraz inhibits fatty acid synthesis through AMPK-S6K1 pathway and LXRg-SREBP-1c pathway in liver.

Description

Dithiolethiones, a novel class of adenosine monophosphate-activated protein kinase (AMPK) activators, prevent insulin resistance through AMPK-dependent p70 ribosomal S6 kinase-1 (S6K1) inhibition. And it is well known that the modulation of S6K1 by oltipraz inhibited the development of insulin resistance and hyperglycemia through the AMPK-S6K1 pathway.Also some research reported that LXRg (a member of the nuclear hormone receptor)-mediated increases in SREBP-1c (the sterol regulatory element-binding protein-1c gene) promote the expression of lipogenic genes and enhance fatty acid synthesis and oltipraz inhibits LXRg and SREBP-c. Therefore, Oltipraz inhibits fatty acid synthesis through AMPK-S6K1 pathway and LXRg-SREBP-1c pathway in liver.

Details
Condition NAFLD, Non-alcoholic Fatty Liver Disease, Nonalcoholic Steatohepatitis (NASH), Nonalcoholic Fatty Liver Disease, Non Alcoholic Fatty Liver Disease, Non-alcoholic Fatty Liver Disease, non-alcoholic fatty liver
Treatment placebos, Oltipraz
Clinical Study IdentifierNCT04142749
SponsorPharmaKing
Last Modified on25 January 2021

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