Abstract
Sleep Apnea-Hypopnea syndrome (OSAS) consists of the total/partial cessation of air flow due to the collapse of the upper airway. Recently, it has been suggested that intermittent hypoxia and sleep fragmentation may play a role in the progression of non-alcoholic fatty liver disease (NAFLD).
We studied the molecular mechanisms that link intermittent hypoxia and sleep fragmentation in liver lipid metabolism. We used mice subjected to intermittent hypoxia protocol or a sleep fragmentation protocol. A histopathological analysis of the livers of these mice was performed by an Hematoxylin/Eosin stain and the lipid content in the liver was measured by an Oil Red O stain. Proteins involved in lipid metabolism were analyzed in the livers of these mice.
Results: The analysis revealed the presence of mild hepatic steatosis in mice subjected to intermittent hypoxia. Similarly, the livers of the mice subjected to sleep fragmentation showed signs of steatosis and inflammation. The Oil Red stain showed that both protocols favored the accumulation of lipids in the liver.
At the molecular level, it was observed that both intermittent hypoxia and sleep fragmentation favored the hepatic expression of the key enzymes in the synthesis of fatty acids (SREBP1, FAS and SCD1), without significantly affecting proteins involved in other essential routes for lipid metabolism in the liver such as beta-oxidation of fatty acids or the capture of the same
Conclusions: Physiopathological characteristics of the OSA, favor the appearance of hepatic steatosis because they induce the expression of genes lipogenic.
Footnotes
Cite this article as: European Respiratory Journal 2019; 54: Suppl. 63, PA873.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
- Copyright ©the authors 2019