Fatty Liver ; drug therapy ; Humans ; Sirtuin 1

Fatty Liver ; drug therapy ; metabolism ; Humans ; Lipid Metabolism ; Lipid Peroxidation

Nonalcoholic fatty liver disease (NAFLD) and hyperhomocysteinemia (HHcy) both are major health problems worldwide, whose incidence are closely related with each other. We previously reported the mechanism of HHcy-caused hepatic steatosis, but the role of n-3 polyunsaturated fatty acid (n-3 PUFA) in HHcy-induced hepatic steatosis remains unclear. In this study, 6-week-old C57BL/6 male mice were given a high methionine diet (HMD, 2% methionine diet), and plasma homocysteine levels were measured by ELISA to confirm the establishment of an HHcy model. Meantime, mice were fed HMD with or without n-3 PUFA supplement for 8 weeks to determine the role and mechanism of n-3 PUFA in hepatic steatosis induced by HHcy. Results showed that n-3 PUFA significantly improved hepatic lipid deposition induced by HHcy. qRT-PCR analysis demonstrated that n-3 PUFA inhibited the upregulation of Cd36, a key enzyme of fatty acid uptake, caused by HHcy. Further, the inhibition of hepatic Cd36 expression was associated with the inactivation of aryl hydrocarbon receptor (Ahr) induced by n-3 PUFA. Of note, mass spectrometry revealed that hepatic content of lipoxin A
Animals ; Fatty Acids, Omega-3 ; Fatty Liver/drug therapy* ; Hyperhomocysteinemia/drug therapy* ; Liver ; Male ; Mice ; Mice, Inbred C57BL

Animals ; Carnitine ; therapeutic use ; Fatty Liver ; drug therapy ; Hepatitis, Viral, Human ; drug therapy ; Humans ; Liver Cirrhosis ; drug therapy

OBJECTIVETo evaluate the efficacy of antioxidants in the treatment of non-alcoholic fatty liver.

METHODSThe Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE or PUBMED (1978-2011), EMBASE (1978-2011), ISI, OVID Database (1978-2011), CNKI Net and WANFANG database (1978-2011) were searched for relevant randomized controlled trials, with also manual search of the bibliographies of the retrieved articles. The data were synthesized to assess the histological response of the patients (hepatic steatosis, inflammation and fibrosis) and hepatic biochemical changes after the treatments (alanine aminotransferase responses).

RESULTSFourteen trials involving 1284 patients were included in the Meta-analysis. The quality of the trials was inconsistent. The data were extracted for meta-analysis or descriptive analysis, which did not yield sufficient evidence that antioxidants could improve hepatic steatosis, inflammation, fibrosis or alanine aminotransferase responses.

CONCLUSIONSThe current data do not support a positive therapeutic effect of antioxidants on nonalcoholic fatty liver, and antioxidants are therefore not recommended in the clinical treatment of the condition.

Adult ; Fatty Liver ; diagnosis ; drug therapy ; Female ; Humans ; Male ; Middle Aged ; Non-alcoholic Fatty Liver Disease ; Waist-Hip Ratio

Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Fatty Liver ; drug therapy ; Humans ; Phytotherapy

Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Fatty Liver ; drug therapy ; prevention & control ; Humans ; Phytotherapy

During chemotherapy in patients with gastrointestinal malignancy, the hepatic lesions may occur as chemotherapy-induced lesions or tumor-associated lesions, with exceptions for infectious conditions and other incidentalomas. Focal hepatic lesions arising from chemotherapy-induced hepatopathies (such as chemotherapy-induced sinusoidal injury and steatosis) and tumor-associated eosinophilic abscess should be considered a mimicker of metastasis in patients with gastrointestinal malignancy. Accumulating evidence suggests that chemotherapy for gastrointestinal malignancy in the liver has roles in both the therapeutic effects for hepatic metastasis and injury to the non-tumor bearing hepatic parenchyma. In this article, we reviewed the updated concept of chemotherapy-induced hepatopathies and tumor-associated eosinophilic abscess in the liver, focusing on the pathological and radiological findings. Awareness of the causative chemo-agent, pathophysiology, and characteristic imaging findings of these mimickers is critical for accurate diagnosis and avoidance of unnecessary exposure of the patient to invasive tissue-based diagnosis and operations.
Abscess ; Diagnosis ; Drug Therapy* ; Eosinophils ; Fatty Liver ; Humans ; Liver ; Neoplasm Metastasis* ; Therapeutic Uses

Lingguizhugan Decoction (LGZG) has been investigated in basic studies, with satisfactory effects on insulin resistance in non-alcoholic fatty liver disease (NAFLD). This translational approach aimed to explore the effect and underlying mechanism of LGZG in clinical setting. A randomized, double-blinded, placebo-controlled trial was performed. A total of 243 eligible participants with NAFLD were equally allocated to receive LGZG (two groups: standard dose and low dose) or placebo for 12 weeks on the basis of lifestyle modifications. The primary efficacy variable was homeostasis model assessment of insulin resistance (HOMA-IR). Analyses were performed in two populations in accordance with body mass index (BMI; overweight/obese, BMI ⩾ 24 kg/m²; lean, BMI < 24 kg/m²). For overweight/obese participants, low-dose LGZG significantly decreased their HOMA-IR level compared with placebo (-0.19 (1.47) versus 0.08 (1.99), P = 0.038). For lean subjects, neither dose of LGZG showed a superior effect compared with placebo. Methylated DNA immunoprecipitation sequencing and real-time qPCR found that the DNA N6-methyladenine modification levels of protein phosphatase 1 regulatory subunit 3A (PPP1R3A) and autophagy related 3 (ATG3) significantly increased after LGZG intervention in overweight/obese population. Low-dose LGZG effectively improved insulin resistance in overweight/obese subjects with NAFLD. The underlying mechanism may be related to the regulation of DNA N6-methyladenine modification of PPP1R3A and ATG3. Lean subjects may not be a targeted population for LGZG.
Humans ; Non-alcoholic Fatty Liver Disease/drug therapy* ; Overweight/drug therapy* ; Insulin Resistance ; Obesity/drug therapy* ; China ; DNA/therapeutic use*