Non-alcoholic Steatohepatitis Clinical Trial
Official title:
Comparison the Effectiveness of L-Carnitine With Atorvastatin in Non-Alcoholic Steatohepatitis (NASH)
The aim of the present study was to compare the effects of simvastatin and L-carnitine coadministration versus simvastatin, L-Carnitine monotherapy on liver transaminases and liver elasticity in NASH patients.
Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of disease ranging from
steatosis to steatohepatitis (nonalcoholic steatohepatitis, NASH) to cirrhosis. Statins are
competitive inhibitors of Hydroxymethylglutaryl-CoA reductase, the rate-limiting step in
cholesterol biosynthesis. They occupy a portion of the binding site of
Hydroxymethylglutaryl-CoA, blocking access of this substrate to the active site on the
enzyme. A reduction in intrahepatic cholesterol leads to an increase in LDL receptor turnover
that results from an enhanced rate of hepatic LDL receptor cycling. On the other hand recent
studies have implicated several important cellular processes and signaling pathways that are
affected by abnormal lipid metabolism, resulting in specific biochemical, histological, and
clinical changes associated with NAFLD.
Maybe statins, as lipid lowering agents, and through their effect in reduction of
intrahepatic cholesterol, can affect the abnormal lipid metabolism in NASH.
L- carnitine, can improve the outcome of NASH, because it reduces lipid levels, limits
oxidative stress, and modulates inflammatory responses . It performs a number of essential
intracellular and metabolic functions, such as fatty acid transport, detoxification of
potentially toxic metabolites, regulation of the mitochondrial acyl-CoA / CoA ratio, and
stabilization of cell membranes. It has a pivotal role in the transport of long chain fatty
acids across the inner mitochondrial membrane.
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