In vitro models of metabolism are powerful tools for discovery, however they are limited by their relatively low metabolic activity and energy expenditure. Metabolic flexibility is a key component of a healthy liver. Dysregulation of hepatic metabolism is linked with lipid accumulation, insulin resistance, and diabetes, due in part to diminished energy expenditure and a lack of AMP-activated protein kinase (AMPK) activity. The primary objective of this research is to develop a model to increase the flux of metabolism in FL83B cells in vitro using beta-guanidinopropionic acid (β-GPA), 1-β-D-ribofuranoside 5-amino-imidazole-4-carboxamide ribose (AICAR), or carbachol. Acute AICAR treatment significantly increased the ADP:ATP ratio, but this impact did not result in acute changes in metabolic flux or chronic changes in gene expression. Acute β-GPA and carbachol treatments did not increase metabolic demand, but chronically, both β-GPA and carbachol increased PGC-1α and perilipin-2 expression.
