Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors investigated the epidemiology of hepatitis C virus (HCV) related to liver diseases in Korea. Anti-HCV was studied by EIA in sera from patients with chronic liver diseases (CLD), individuals at high risk, healthy individuals, and family members of patients with CLD. We also evaluated the efficacy of a new anti-HCV assay kit, HCD EIA, consisting of 3 recombinant peptides derived from CORE, NS3 and NS5 regions of the HCV genome, for screening HCV infection. The prevalence of anti-HCV in HCD EIA was 15.4% of 1055 cases studied, while that in the anti-C100-3 EIA was 11.1%. The incidence of anti-HCV in HCD EIA was 5.9% of 17 cases with acute hepatitis, 18.1% of 293 cases with chronic hepatitis, 24.1% of 79 cases with liver cirrhosis, 28.0% of 100 cases with hepatocellular carcinoma, 19.8% of 81 cases maintained with hemodialysis, 31.3% of 16 cases with blood dyscrasias, 4.4% of 114 cases with fatty liver, 1% of 100 healthy persons, 1.3% of 150 blood donors, and 6.2% of 97 family members from 26 patients with type C CLD. Familial HCV clustering was detected in 3 (11.5%) of 26 patients with anti-HCV(+) CLD. The prevalence of anti-HCV in 190 HBsAg positive CLD was 8.4%. The relative proportions of positive anti-HCV, HBsAg, both positive 17.4%, 40.7%, and 3.7%, respectively, while 38.2% of the cases were negative for both anti-HCV and HBsAg. The prevalence of anti-HCV among CLD increased significantly in relation to age (p < 0.05), and it became higher than that of HBsAg after age 60.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevalence of hepatitis C virus related to liver diseases in Korea. 768 3

Chronic feeding of HCD (high-carbohydrate diet) is one of the major contributors to the prevailing of metabolic diseases. ATF4 (activating transcription factor 4) has been shown to play an important role in the regulation of glucose metabolism and obesity development; however, it is unclear how ATF4(-/-) mice respond to HCD. In the present study, we show that 8 weeks of HCD results in significant higher accumulation of TAGs (triacylglycerols) in livers and impairment in glucose tolerance in ATF4(+/+) mice, but not in ATF4(-/-) mice, compared with those on a normal diet. Meanwhile, energy expenditure is further enhanced by HCD in ATF4(-/-) mice. Moreover, we show that ATF4 deficiency suppresses HCD-induced SCD1 (stearoyl-CoA desaturase 1) expression, furthermore, oral supplementation of the main product of SCD1 oleate (18:1) increases TAG accumulation in livers of ATF4(-/-) mice. Taken together, these results suggest that ATF4 deficiency is protective for HCD-induced hepatic steatosis and impairment of glucose tolerance and insulin sensitivity. Furthermore, the resistance to hepatic steatosis is at least in part due to suppression of SCD1 expression under HCD.
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PMID:ATF4 deficiency protects mice from high-carbohydrate-diet-induced liver steatosis. 2164 28

The incidence of non-alcoholic steatohepatitis (NASH) is increasing. Because gut microbiota have been highlighted as one of the key factors in the pathogenesis of metabolic syndrome, we investigated the involvement of the bacterial component in the progression of non-alcoholic fatty liver (NAFL) to NASH. C57BL/6 mice were fed with maintenance food (MF, groups A and B) or a high caloric diet (HCD, groups C and D) for 1 month. Mice were then divided into four groups: Groups A and C were inoculated with PBS, while groups B and D were inoculated with lipopolysaccharide (LPS) plus complete Freund's adjuvant (CFA). The inoculations were performed a total of 3 times over 3 months. At 6 months, while hepatic steatosis was observed in groups C and D, cellular infiltration and fibrosis were less evident in group C than in group D. Inflammatory cytokines were upregulated in groups B and D. 16S rRNA pyrosequencing of whole colon homogenates containing faeces showed that certain bacterial groups, such as Bacteroidaceae, Peptostreptococcaceae and Erysipelotrichaceae, were increased in groups C and D. Although loading of bacterial components (LPS) resulted in hepatic inflammation in both MF- and HCD-fed mice, HCD feeding was more crucial in the progression of NAFL during the triggering phase.
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PMID:Effect of Lipopolysaccharide on the Progression of Non-Alcoholic Fatty Liver Disease in High Caloric Diet-Fed Mice. 2652 7

Dietary betaine supplementation notably ameliorated fatty liver disease caused by high dietary carbohydrate. We hypothesised that the mechanism behind this is the alteration of bile acid and trimethylamine-N-oxide (TMAO) metabolism. We further explored this mechanism by supplementing betaine (1%) to the diet of a farmed fish Megalobrama amblycephala. Four diet groups were designed: control (CD, 27.11% carbohydrates), high-carbohydrate (HCD, 36.75% carbohydrates), long-term betaine (HCB, 35.64% carbohydrates; 16 weeks) and short-term betaine (HC4B; 12 weeks HCD + 4 weeks HCB) diets. We analysed the histology of the liver (hematoxylin and eosin staining), the metabolites related to TMAO in plasma (high-performance liquid chromatography-tandem mass spectrometry), the expression of the relative gene in the liver and gut microbiota (qPCR), and the composition of gut microbiota (terminal restriction fragment length polymorphism). HCD elevated lipid accumulation in the liver and decreased the gene expression of bile acid transport, trimethylamine (TMA) formation and the diversity of gut microbiota compared to CD. HCB reversed these patterns, and elevated the gene expression of bile acid receptors and decreased the total cholesterol and TMAO concentration (all compared to HCD). HCD and HCB both increased the gene expression of bile acid synthesis (all p < 0.05). In conclusion, we hypothesise that HCB decreased liver lipid accumulation caused by a high-carbohydrate diet through improvement of the gut microbial community (the diversity of gut microbiota), TMA formation (the expression of associated microbial genes and bacterial taxa), TMAO metabolism (the formation of TMAO) and bile acid metabolism (the gene expression of the synthesis and transport of bile acids and their receptors). HC4B produced intermediate effects of those between HCD and HCB.
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PMID:Dietary betaine reduces liver lipid accumulation via improvement of bile acid and trimethylamine-N-oxide metabolism in blunt-snout bream. 3155 7

MicroRNAs are well acknowledged as key mediators in the development of chronic metabolic diseases, including NAFLD. However, their roles in hepatic lipid metabolism and fatty liver still remain well elucidated. Here, we found that miR-103 represses de novo lipogenesis (DNL) and dampens the development of obesity/diet-induced fatty liver through targeting at Fasn and Scd1 in mouse liver. miR-103, robustly amplified in obese livers, inhibits the expression of Fasn and Scd1 via directly interacting with their mRNA 3' untranslated regions. Upregulated miR-103 sufficiently reduces the expression of Fasn and Scd1 and blocks the lipid accumulation in oleate-incubated hepatocytes. Furthermore, specifically overexpressing miR-103 in mouse liver by adenovirus significantly inhibits hepatic DNL to repress HCD-promoted hepatic lipid contents as well as NAFLD development. Meanwhile, enforced expression of hepatic miR-103 also alleviates obesity-associated fatty liver via reducing Fasn and Scd1 in db/db mice. Together, our study reveals a critical role of miR-103 in lipid homeostasis of liver and pathogenesis of NAFLD.
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PMID:MicroRNA-103 represses hepatic de novo lipogenesis and alleviates NAFLD via targeting FASN and SCD1. 3203 13