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Adipokines and Pathogenesis of Non Alcoholic Fatty Liver Disease. Edition No. 1

  • ID: 1905491
  • October 2008
  • 192 Pages
  • VDM Publishing House
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Non alcoholic fatty liver disease is the hepatic
manifestation of metabolic syndrome that may
progress from simple steatosis to nonalcoholic
steatohepatitis, cirrhosis and hepatocellular
carcinoma. Expansion of omental adipose is
accompanied by alteration in profiles of
adipocytokines that contribute to NAFLD through
enhanced steatogenesis in the liver and its
inflammation. Gene transcription studies
demonstrated a prominent adipose-specific
deregulation of the inflammation and immune system
related genes in NASH. Serum levels
of soluble adipokines and cytokines can reliably
predict NASH in the cohort of morbidly obese
patients. Histologic fibrosis in patients with NASH
could be predicted by TNF-? level. There is also
strong connection between the HCV genotype 3,
steatosis and increases in IL-8 serum levels. HCV
genotype specific differences in soluble cytokine
concentrations may help to elucidate pathogenesis of
HCV hepatitis and potential triggers for HCV-related
steatosis. These results should be of interest to
the researchers of the clinical and fundamental
aspects of human metabolism, obesity, diabetes, and
hepatitis C.

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Mohammed Jarrar.
Mohammed H. Jarrar, PhD,MT. Assistant Professor of Biosciences
at Biology Department, George Mason University, RAK-UAE. Studied
CRA at George Washington University, Biotechnology at Johns
Hopkins and George Mason universities. Worked as CLS at Hopkins
Pathology for 10 years and for 2 years as Senior Researcher at
KKI, Baltimore, USA.

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