Fimasartan Ameliorates Nonalcoholic Fatty Liver Disease through PPARδ Regulation in Hyperlipidemic and Hypertensive Conditions

Serum aminotransferases in nonalcoholic fatty liver disease are a signature of liver metabolic perturbations at the amino acid and Krebs cycle level1,2

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Pathophysiology of Non Alcoholic Fatty Liver Disease

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AMPK: A cellular metabolic and redox sensor. A minireview

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Influence of Hepatic Dysfunction on the Pharmacokinetics and Safety of Fimasartan

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Berberine metabolites exhibit triglyceride-lowering effects via activation of AMP-activated protein kinase in Hep G2 cells

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The effects of running exercise on oxidative capacity and PGC-1α mRNA levels in the soleus muscle of rats with metabolic syndrome

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AMPK activation, a preventive therapeutic target in the transition from cardiac injury to heart failure

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Effect of age on the pharmacokinetics of fimasartan (BR-A-657)

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Secondary causes of nonalcoholic fatty liver disease

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Globular adiponectin regulates energy homeostasis through AMP-activated protein kinase–acetyl-CoA carboxylase (AMPK/ACC) pathway in the hypothalamus

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Telmisartan attenuates progression of steatohepatitis in mice: role of hepatic macrophage infiltration and effects on adipose tissue

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AMPK and PPARδ Agonists Are Exercise Mimetics

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The establishment of a novel non-alcoholic steatohepatitis model accompanied with obesity and insulin resistance in mice

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Nonalcoholic fatty liver disease and mitochondrial dysfunction

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