Figure 1

Exogenous LPA inhibits glucagon-stimulated glucose production in primary hepatocytes. (A) Basal and glucagon-stimulated glucose production from WT primary hepatocytes after 13 hrs in glucose-free DMEM in the absence or presence of LPA at 0.4, 2.5, and 10 μM; n = 5–6. Glucose released into the media (ng glucose/mg hepatocyte protein) was normalized to the vehicle control. (B) Gluconeogenic gene expression of WT hepatocytes after 13 hrs in glucose-free DMEM in the absence or presence of LPA (2.5 μM), glucagon (10 nM) and/or insulin (100 nM); n = 3. (C) Representative Western blot and quantification of PEPCK expression in WT primary hepatocytes treated for 13 hrs with LPA, glucagon and/or insulin, with 14-3-3 as a loading control; n = 4. All data are means ± standard error of the mean (SEM). For A–C, p < 0.05 by one-way ANOVA compared to vehicle control (#) or glucagon control (*). For C, the ANOVA was run with the following multiple comparisons: vehicle vs. glucagon and glucagon vs. glucagon + LPA. ns, not significant.