Direct actions of GLP-1 analogues on AMP-activated protein kinase activity are distinct from cyclic AMP accumulation

Regarding the publication by Ben-Shlomo et al. [1], the authors present data supporting the role of the incretin hormone glucagon-like peptide 1 (GLP-1) for decreased hepatic steatosis. They use a rat model with dipeptidyl peptidase 4 (DPP4) deficiency which decreases GLP-1 degradation and raises circulating endogenous GLP-1 levels by more than 3-fold. They observe a reduction in liver triglyceride in concert with decreased hepatic transcript levels of lipogenic genes. These findings are consistent with data from other laboratories using GLP-1 and related analogues, as well as DPP4 inhibition, in rodent models of hepatic steatosis [2–5].