Related Experiment Video
Updated: May 18, 2026

An Experimental Model of Diet-Induced Metabolic Syndrome in Rabbit: Methodological Considerations, Development, and Assessment
Published on: April 20, 2018
[Pathogenetic therapy of metabolic syndrome at the stage of visceral lesions]
Abstract:
Insulin resistance and oxidative stress play an important role in the pathogenetic mechanism of non-alcoholic fatty liver disease. Hepatoprotective therapy that blocks the second phase of pathogenesis (oxidative stress) is a promising modality for the treatment of non-alcoholic steatohepatitis (NACH). An alternative approach is the use of medicines recovering the mitochondrial membrane, lipid bi-layer of the plasma membrane, oxidative phosphorilation, and cellular metabolism. In this context, succinic acid-based remaxol showing antioxidative, antihypoxic and cytoprotective activities can be regarded as a promising metabolic hepatoprotector for the treatment of non-alcoholic fatty liver disease. The present original study demonstrated the clinical efficacy of remaxol in pathogenetic therapy of NACH in patients with metabolic syndrome. Its introduction in the combined treatment of NACH increased functional capacity of the liver by decreasing the severity of cytolysis, cholestasis, hepatomegalia, and steatosis (ultrasonic study), improved lipid metabolism, reduced cholesterol level, triglyceridemia, and atherogenic index. Remaxol exerted nephroprotective action in patients with diabetic nephropathy at stage 1 of chronic renal insufficiency (increased glomerular filtration rate and decreased blood creatinine level). The study demonstrated the advantage of medications with antihypoxic properties over traditional therapy of NACH.
Insights
Remaxol, a succinic acid-based drug, effectively treats non-alcoholic steatohepatitis (NACH) by combating oxidative stress and improving liver function. This metabolic hepatoprotector also shows benefits for kidney function in patients with diabetic nephropathy.
Area of Science:
- Hepatology
- Metabolic Syndrome
- Oxidative Stress
Background:
- Non-alcoholic fatty liver disease (NAFLD) pathogenesis involves insulin resistance and oxidative stress.
- Targeting oxidative stress (the second phase of NAFLD pathogenesis) offers a promising therapeutic strategy.
- Restoring mitochondrial and cellular functions presents an alternative treatment approach.
Purpose of the Study:
- To evaluate the clinical efficacy of remaxol, a succinic acid-based metabolic agent, in the pathogenetic therapy of non-alcoholic steatohepatitis (NACH).
- To assess remaxol's impact on liver function, lipid metabolism, and renal function in patients with NACH and metabolic syndrome.
Main Methods:
- Original clinical study involving patients with NACH and metabolic syndrome.
- Assessment of liver function through ultrasound to evaluate cytolysis, cholestasis, hepatomegaly, and steatosis.
- Monitoring of lipid metabolism parameters (cholesterol, triglycerides, atherogenic index) and renal function (glomerular filtration rate, creatinine).
Main Results:
- Remaxol improved liver function by reducing cytolysis, cholestasis, hepatomegaly, and steatosis.
- Treatment with remaxol led to improvements in lipid metabolism, lowering cholesterol, triglyceridemia, and the atherogenic index.
- Remaxol demonstrated nephroprotective effects in patients with diabetic nephropathy, improving glomerular filtration rate and reducing blood creatinine.
Conclusions:
- Remaxol is an effective metabolic hepatoprotector for NACH, offering advantages over traditional therapies.
- Succinic acid-based medications with antihypoxic properties show promise in managing NACH.
- Remaxol exhibits a dual benefit, improving both liver and kidney function in relevant patient populations.
Related Concept Videos
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis II: Pathophysiology
Chronic Pancreatitis II: Pathophysiology
Type II Diabetes II: Pathophysiology
Atherosclerosis III: Management
Type I Diabetes II: Pathophysiology