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| variceal bleeding, chronic, plump moms , real plump , arteriosclerosis, plump furries , fats, choline deficiency, infected, girls with fat ass , fatty fat fat , plump white , rapid fulminant liver failure, methadone, nonalcoholic, ribivirin, big and plump , | Ultimately, the future for potential therapeutic modalities to treat white girls with fat asses this disease are quite promising, but further research is needed to clearly demonstrate which therapy or therapies will be effective at white girls with fat asses eliminating fatty liver disease and its potential complications.Publication Types: Review PMID: 14609346 [PubMed - indexed for MEDLINE] Display Summary Brief Abstract Citation MEDLINE XML UI List LinkOut ASN.1 Related Articles Cited Articles Cited white girls with fat asses in Books CancerChrom Links Domain Links 3D Domain Links GEO DataSet Links Gene Links Gene (GeneRIF) Links Genome Links Project Links GENSAT Links GEO Profile Links HomoloGene Links Nucleotide Links OMIA Links OMIM (calculated) Links OMIM (cited) Links BioAssay Links Compound Links Compound via MeSH Substance Links Substance via MeSH PMC Links Cited in PMC PopSet Links Probe Links Protein Links SNP Links Structure Links UniGene Links UniSTS Links Show 5 10 20 50 100 200 500 Sort by Pub Date First Author Last Author Journal Send to Text File Printer Clipboard E-mail Order |
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| Most patients are asymptomatic and usually present with mild elevations in aminotransferases. The natural history of NAFLD is not clearly defined but progression to cirrhosis and end-stage liver disease is arteriosclerosis well recognised in some patients. The accumulation arteriosclerosis of hepatic steatosis is thought to occur initially, primarily through hepatic and peripheral insulin resistance, which leads to altered glucose and free fatty acid metabolism. The progression from simple fatty liver to more severe forms of NAFLD (nonalcoholic steatohepatitis and cirrhosis) is arteriosclerosis much less clear but evidence suggests that oxidative stress may preferentially enhance proinflammatory cytokines, which leads to cellular adaptations and dysfunction followed by development of inflammation, necrosis and fibrosis. Therapeutic modalities remain limited and are largely focused on correcting the underlying insulin resistance or reducing oxidative stress. However, at the present time, there are several limitations to the current potential therapies, mainly because of the lack of large-scale, prospective, randomised studies, as well as clearly defined histological endpoints. |
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