The Crosstalk between Hypoxia and Innate Immunity in the Development of Obesity-Related Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) has become a major health issue in western countries in parallel with the dramatic increase in the prevalence of obesity and all obesity related conditions, including respiratory diseases as obstructive sleep apnea-hypopnea syndrome (OSAHS). Interestingly, th...

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Bibliographic Details
Published in:BioMed research international 2015-01, Vol.2015 (2015), p.1-8
Main Authors: Crespo, Javier, Lόpez Hoyos, Marcos, Fábrega, Emilio, Arias-Loste, María Teresa
Format: Article
Language:English
Subjects:
Animals
Body mass index
Cytokines
Development and progression
Hospitals
Humans
Hypoxia
Hypoxia - immunology
Hypoxia - pathology
Hypoxia-Inducible Factor 1 - immunology
Immune response
Immunity, Innate
Infections
Inflammation
Insulin resistance
Lipids
Liver
Liver - immunology
Liver - pathology
Liver diseases
Metabolism
NF-kappa B - immunology
Non-alcoholic Fatty Liver Disease - etiology
Non-alcoholic Fatty Liver Disease - immunology
Non-alcoholic Fatty Liver Disease - pathology
Obesity
Obesity - complications
Obesity - immunology
Obesity - pathology
Observations
Pathogenesis
Physiological aspects
R&D
Research & development
Review
Rodents
Sleep Apnea, Obstructive - etiology
Sleep Apnea, Obstructive - immunology
Sleep Apnea, Obstructive - pathology
Transcription factors
Tumor necrosis factor-TNF
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Summary:Nonalcoholic fatty liver disease (NAFLD) has become a major health issue in western countries in parallel with the dramatic increase in the prevalence of obesity and all obesity related conditions, including respiratory diseases as obstructive sleep apnea-hypopnea syndrome (OSAHS). Interestingly, the severity of the liver damage in obesity-related NAFLD has been associated with the concomitant presence of OSAHS. In the presence of obesity, the proinflammatory state in these patients together with intermittent episodes of hypoxia, characteristic of OSAHS pathogenesis, may lead to an enhanced inflammatory response mediated by a positive feedback loop mechanism that implicates HIF-1 and NFκB. Thus, the severity of liver involvement in obese NAFLD patients with a concomitant diagnosis of OSAHS could be explained. In this review, we focus on the molecular mechanisms underlying the hepatic response to chronic intermittent hypoxia and its interaction with innate immunity in obesity-related NAFLD.
ISSN:2314-6133
2314-6141
DOI:10.1155/2015/319745