METHODS: The hypothesis was clinical proteomics tests

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plump lip , tests, dosing, symptoms, plump mature , treatments for nonalcoholic fatty liver diseasee, fatty ass , fatty acid definition , hep c, n 3 polyunsaturated fatty acids , combo, maldi, encephalopathy, hepatitis a, copegus, hcv drug, hcv medication, liver, plump dj , for both steps). Although baseline rates of glycerol appearance were higher in those with NASH than in those with fatty liver clinical proteomics (means, 14.6 vs. 21.6 micromol. kg(-1). min(-1); P < 0.05), neither group significantly clinical proteomics suppressed glycerol appearance at insulin infusion rates of 10 clinical proteomics mU. m(-2). min(-1). NASH was associated with loss of mitochondrial cristae and paracrystalline inclusions in 9 of 10 subjects, compared with 0 of 6 subjects with fatty liver. However, no evidence of a generalized defect in fatty acid beta oxidation was noted in any group. Also, mean [beta-OH butyrate] was highest in those with NASH (means, 90 vs.
METHODS: The hypothesis was tested by evaluation of (1) insulin resistance by a 2-step hyperinsulinemic (10 and 40 mU. m(-2). min(-1)) euglycemic clamp; (2) tests insulin effects on lipolysis by enrichment of [U-(13)C]glycerol; (3) frequency and severity of tests structural defects in hepatocyte mitochondria in vivo; (4) fatty acid beta oxidation from serum [beta-OH butyrate], release of water-soluble radioactivity from (3)H-palmitate by cultured fibroblasts and urinary dicarboxylic acid excretion; and (5) hepatic lipid peroxidation by immunohistochemical staining for 3-nitrotyrosine (3-NT). Subjects with NASH (n = 6-10 for different studies) were compared with those with fatty liver (n = 6) or tests normal controls (n = 6). RESULTS: NASH and fatty liver were both associated with insulin resistance, with mean glucose infusion rates (normal/fatty liver/NASH) of step 1, 4.5/1.6/0.9; step 2, 9.5/7.7/4.5 (P < 0.03
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