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Pathophysiology of Nonalcoholic Steatohepatitis (Paperback)
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Pathophysiology of Nonalcoholic Steatohepatitis (Paperback)
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Rapid advances on molecular studies, manipulation of the mouse
genome, the development of a number of animal models, and using
these in studies of nonalcoholic fatty liver disease (NAFLD) have
provided important insights into the pathogenesis of this
relatively common disorder. One of the most crucial advances was to
recognise the links among obesity, insulin resistance, inflammation
and NAFLD. A growing body of literature has shown that insulin
resistance and its liver-related consequence, NAFLD, could be the
result of generalised inflammation. Genetic and behavioral factors
contribute to increased visceral adipose tissue where increased
oxidative stress and lipid peroxidation may contribute to
dysregulated production of adipocytokines, fatty acids, and
bioactive lipids. This chain of these events may contribute to
local and peripheral insulin resistance, a central underlying
pathophysiological process that may both cause and result from
increased peripheral lipolysis and elevated free fatty acid
concentrations in the circulation. Abnormally elevated free fatty
acids taken up by organs other than adipose tissue, such as liver
and skeletal muscle, contributes to steatosis of these organs
(ectopic lipogenesis). Increased muscle and hepatocellular lipid
content provides substrates for oxidative stress and lipid
peroxidation, and also promotes insulin resistance in both liver
and muscle by disturbing their downstream insulin signaling
cascades. Insulin resistance further increases peripheral lipolysis
in adipose tissue, further elevates circulating free fatty acids,
inhibits hepatic fatty acid a-oxidation and increases de novo
synthesis of both fatty acids and triglycerides in the liver.
Excessively produced triglycerides in the liver are either stored
as fat droplets or secreted into the plasma as very-low-density
lipoproteins. If this complex mechanism of hepatic fat synthesis
and secretion capacity is overwhelmed, excessive triglycerides
accumulate within the hepatocytes and manifests as NAFLD. A fatty
liver is sensitive to hepatocellular injury and sustained injury
can manifest as nonalcoholic steatohepatitis (NASH),
NASH-associated cirrhosis, and NASH-associated hepatocellular
carcinoma. Specific depletion of hepatic natural killer T cells
with consequent proinflammatory cytokine polarisation of liver
cytokine production might be one reason for this increased hepatic
sensitivity against various stimuli. Only a minority of patients
with NAFLD have the necroinflammatory changes of NASH. The
development of NASH in patients with NAFLD may be the consequence
of secondary abnormalities such as injured and dysfunctional
mitochondria, generation of reactive oxygen species with
down-regulation or consumption of antioxidants causing oxidative
stress and lipid peroxidation, increased activity of cytochrome
P450 2E1, disturbed production of adipocytokines, and the effects
of gut-derived cytotoxic products. The dynamic interplay of these
processes in the pathogenesis of NAFLD remains incompletely
understood and is an area of active research.
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