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Nonalcoholic fatty liver disease: the pathogenetic roles of insulin resistance and adipocytokines.

TitleNonalcoholic fatty liver disease: the pathogenetic roles of insulin resistance and adipocytokines.
Publication TypeJournal Article
Year of Publication2009
AuthorsPolyzos, S. A., Kountouras J., & Zavos C.
JournalCurr Mol Med
Volume9
Issue3
Pagination299-314
Date Published2009 Apr
ISSN1566-5240
KeywordsAdipokines, Adiponectin, Fatty Acids, Nonesterified, Fatty Liver, Humans, Insulin, Insulin Resistance, Leptin, Oxidative Stress, Signal Transduction, Tumor Necrosis Factor-alpha
Abstract

Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of common hepatic disorders in western countries, with multiple consequences and its incidence is paralleling the increasing numbers of overweight and obese individuals worldwide. The pathogenesis of NAFLD is thought to be related mainly with insulin resistance (IR) syndrome and oxidative stress; the latter resulting from mitochondrial fatty acids (FFAs) oxidation, nuclear factor-kappaB (NFkappaB)-dependent inflammatory cytokine expression and adipocytokines may promote hepatocellular damage, inflammation, fibrosis and progressive liver disease. Adipocytokines and other recognized cytokines produced partially by inflammatory cells infiltrating adipose tissue, play an important role in the pathogenesis of IR and NAFLD, through complex and interactive paracrine and endocrine mechanisms. Some adipocytokines, including adiponectin and leptin decrease IR, while others, including tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and resistin enhance IR. The multi-hit hypothesis provides a model that summarizes the complex factors and interactions leading from adipocytokines, FFAs metabolism and IR to NAFLD. This review outlines the pathways involved in adipocytokines, IR and NAFLD sequence; the first part describes the impaired IR pathway leading to NAFLD and the second part the mechanisms by which adipocytokines influence IR and NAFLD development and progression. Understanding these complex mechanisms has evoked new therapeutic approaches, which may provide promising results to date.

DOI10.2174/156652409787847191
Alternate JournalCurr. Mol. Med.
PubMed ID19355912

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