MicroRNA-194 inhibition improves dietary-induced non-alcoholic fatty liver disease in mice through targeting on FXR
Hezhongrong NieChunli SongDaming WangShengjin CuiTingyu RenZhaopeng CaoQing LiuZeyan ChenXiaoyong ChenYiwen Zhou
48
Citation
24
Reference
10
Related Paper
Citation Trend
Keywords:
Steatosis
To study the relationship between non-alcoholic fatty liver disease and insulin resistance.63 non-alcoholic fatty liver disease patients(male 35,femal 28) and 20 obesity without fatty liver disease were selected.Fasting serum insulin levels was measured by radio-immunoassay,insulin resistance index was estimated by the homeostasis model assessment(HOMA-IR).Compared to controlgroup,patients with non-alcoholic fatty liver disease were characterized by hyperinsluinemia,elevated insulin resistance index(P0.01).Serum insulin and insulin resistance index were higher in heavy fatty liver disease patients than medium and light patients(P0.05).In the pathogeneses of non-alcoholic fatty liver disease,insulin resistance was an original factor probably and not a following changing.
Alcoholic fatty liver
Liver disease
Cite
Citations (0)
Steatosis
Liver steatosis
Cite
Citations (2)
Two distinct forms of hepatocellular steatosis can be seen in patients with chronic hepatitis C virus (HCV) infection. Classical metabolic risk factors for hepatocellular steatosis account for the vast majority of cases of steatosis in patients infected by non-genotype 3 HCV strains. In contrast, in patients infected by HCV genotype 3, steatosis is generally induced by the virus itself through a direct cytopathic effect, the mechanisms of which remain debated. Mixed forms of steatosis can also be seen in HCV genotype 3-infected patients with metabolic risk factors. Hepatocellular steatosis appears to be associated with more rapid progression of hepatic fibrosis. However, it is unclear whether this association is due to steatosis itself, or rather to metabolic and host factors that promote steatosis and fibrosis concomitantly. This review discusses current knowledge of HCV-induced steatosis and its relation to chronic HCV-associated liver disease.
Steatosis
Hepatitis C
Cite
Citations (79)
Keywords: Insulin resistance; Metabolic score for insulin resistance; Homeostatic model assessment for insulin resistance; Non-alcoholic fatty liver disease; Fatty liver
Homeostasis
Homeostatic model assessment
Cite
Citations (1)
Non-alcoholic fatty liver disease (NAFLD) was redefined as metabolic dysfunction-associated fatty liver disease (MAFLD) in 2020. Due to this, further validation of the non-invasive tests used in NAFLD diagnosis is required for MAFLD. There are five known steatosis indices for computed tomography (CT)-diagnosed MAFLD. These indices include the fatty liver index (FLI), the hepatic steatosis index (HSI), the lipid accumulation product (LAP), the visceral adiposity index (VAI), and the Zhejiang University index (ZJU). We aimed to analyze the diagnostic abilities of these five widely known steatosis indices for CT-diagnosed MAFLD. From March 2012 to October 2019, we retrospectively analyzed the clinical information and images of 1300 adults aged ≥19 years who underwent CT scans at our institution. To compare differences, the Chi-square test and independent
Steatosis
Cite
Citations (22)
Li, Xiaoyan; Wang, Xiaofang; Jiang, Li; Harris, Peter C.; Li, Xiaogang; Torres, Vicente E. Author Information
Cite
Citations (0)
Cite
Citations (3)
Cancer cells differ from normal cells in both gain of functions (i.e., upregulation) and loss of functions (i.e., downregulation). While it is common to suppress gain of function for chemotherapy, it remains challenging to target downregulation in cancer cells. Here we show the combination of enzyme-instructed assembly and disassembly to target downregulation in cancer cells by designing peptidic precursors as the substrates of both carboxylesterases (CESs) and alkaline phosphatases (ALPs). The precursors turn into self-assembling molecules to form nanofibrils upon dephosphorylation by ALP, but CES-catalyzed cleavage of the ester bond on the molecules results in disassembly of the nanofibrils. The precursors selectively inhibit the cancer cells that downregulate CES (e.g., OVSAHO) but are innocuous to a hepatocyte that overexpresses CES (HepG2), while the two cell lines exhibit comparable ALP activities. This work illustrates a potential approach for the development of chemotherapy via targeting downregulation (or loss of functions) in cancer cells.
Dephosphorylation
Cite
Citations (135)
Abstract Background: Steatosis is diagnosed on the basis of the macroscopic aspect of the liver evaluated by the surgeon at the time of organ extraction or by means of a frozen biopsy. Aim: In the present study, the applicability of laser‐induced fluorescence (LIF) spectroscopy was investigated as a method for the diagnosis of different degrees of steatosis experimentally induced in rats. Material and methods: Rats received a high‐lipid diet for different periods of time. The animals were divided into groups according to the degree of induced steatosis diagnosis by histology. The concentration of fat in the liver was correlated with LIF by means of the steatosis fluorescence factor (SFF). Results: The histology classification, according to liver fat concentration was, Severe Steatosis, Moderate Steatosis, Mild Steatosis and Control (no liver steatosis). Fluorescence intensity could be directly correlated with fat content. It was possible to estimate an average of fluorescence intensity variable by means of different confidence intervals ( P =95%) for each steatosis group. SFF was significantly higher in the Severe Steatosis group ( P <0.001) compared with the Moderate Steatosis, Mild Steatosis and Control groups. Conclusion: The various degrees of steatosis could be directly correlated with SFF. LIF spectroscopy proved to be a method capable of identifying the degree of hepatic steatosis in this animal model, and has the potential of clinical application for non‐invasive evaluation of the degree of steatosis.
Steatosis
Liver steatosis
Histology
Cite
Citations (19)
"Downregulation of miR-140-3p Is a Cause of Upregulation of RhoA Protein in Bronchial Smooth Muscle of Murine Experimental Asthma." American Journal of Respiratory Cell and Molecular Biology, 64(1), pp. 138–140
Cite
Citations (7)