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Evidence for AMPK-dependent regulation of exocytosis of lipoproteins in a model liver cell line
Journal article   Peer reviewed

Evidence for AMPK-dependent regulation of exocytosis of lipoproteins in a model liver cell line

Livia Puljak, Vinay Parameswara, Svjetlana Dolovcak, Shar L Waldrop, Daniel Emmett, Victoria Esser, J. Gregory Fitz and Gordan Kilic
Experimental cell research, Vol.314(10), pp.2100-2109
2008
DOI: 10.1016/j.yexcr.2008.03.002
PMCID: PMC2699465
PMID: 18405894
url
https://www.ncbi.nlm.nih.gov/pmc/articles/2699465View
Open Access

Abstract

5′-AMP-activated kinase (AMPK) plays a key role in the regulation of cellular lipid metabolism. The contribution of vesicular exocytosis to this regulation is not known. Accordingly, we studied the effects of AMPK on exocytosis and intracellular lipid content in a model liver cell line. Activation of AMPK by metformin or 5-aminoimidazole-4-carboxamide-1-beta- d-ribofuranoside (AICAR) increased the rates of constitutive exocytosis by about 2-fold. Stimulation of exocytosis by AMPK occurred within minutes, and persisted after overnight exposure to metformin or AICAR. Activation of AMPK also increased the amount of triacylglycerol (TG) and apolipoprotein B (apoB) secreted from lipid-loaded cells. These effects were accompanied by a decrease in the intracellular lipid content indicating that exocytosis of lipoproteins was involved in these lipid-lowering effects. While AMPK increased the rates of fatty acid oxidation (FAO), the lipid-lowering effects were quantitatively significant even after inhibition of FAO with R-etomoxir. These results suggest that hepatic AMPK stimulates constitutive exocytosis of lipoproteins, which may function in parallel with FAO to regulate intracellular lipid content.
Nile red AMPK FM1-43 Constitutive exocytosis Intracellular lipids

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