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vs. 0.95 ± 0.06, respectively; P = 0.429) and larger than control subjects (0.83 ± fatty vautin 0.09; P = 0.02). In summary, NAFLD patients, even in the presence of normal body weight, have a relatively increased visceral adiposity, which might be relevant in the pathogenesis of their liver disease. Whatever the cause of hepatic lipid deposition, it may remain clinically undetectable or may cause disorders from ongoing liver damage to terminal liver failure needing hepatic transplantation. To explain differences between pure fatty liver and NASH, Day and James (41) proposed a "two-hit hypothesis," with lipids fatty vautin acting as the first "hit" fatty vautin and increased lipid peroxidation being the second "hit." To explain oxidative stress, another culprit may be present but not necessarily the same agent in all cases.
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