Inhibition of exendin-4-induced steatosis by protein kinase A in cultured HepG2 human hepatoma cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2017-07-13

AUTHORS

Alice Y. Chen-Liaw, Gabrielle Hammel, George Gomez

ABSTRACT

Nonalcoholic fatty liver is characterized by the abnormal accumulation of triglycerides within hepatocytes, resulting in a steatotic liver. Glucagon-like peptide 1 and its analog exendin-4 can ameliorate certain aspects of this syndrome by inducing weight loss and reducing hepatic triglyceride accumulation, but it is unclear whether these effects result from the effects of glucagon-like peptide 1 on the pancreas, or from direct action on the liver. This study investigated the direct action and putative cellular mechanism of exendin-4 on steatotic hepatocytes in culture. Steatosis was induced in cultured HepG2 human hepatoma cells by incubation in media supplemented with 2 mM each of linoleic acid and oleic acid. Steatotic hepatocytes were then pre-incubated in the protein kinase A inhibitor H89 for 30 min, then treated with exendin-4 over a period of 24 h. Cell viability and triglyceride content were characterized by a TUNEL assay and AdipoRed staining, respectively. Our results showed that steatotic cells maintained high levels of intracellular triglycerides (80%) compared to lean controls (25%). Exendin-4 treatment caused a significant reduction in intracellular triglyceride content after 12 h that persisted through 24 h, while protein kinase A inhibitors abolished the effects of exendin-4. The results demonstrate the exendin-4 induces a partial reduction in triglycerides in steatotic hepatocytes within 12 h via the GLP-1 receptor-mediated activation of protein kinase A. Thus, the reduction in hepatocyte triglyceride accumulation is likely driven primarily by downregulation of lipogenesis and upregulation of β-oxidation of free fatty acids. More... »

PAGES

721-727

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11626-017-0181-y

DOI

http://dx.doi.org/10.1007/s11626-017-0181-y

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1090661270

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28707223


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