Preliminary analysis of mean and standard error of fasting blood glucose concentrations in five groups of mice (n = 10/group). Asterisks indicate significance in a multivariate linear model with covariates (***P < 0.001, **P < 0.01, *P < 0.05). (Diet control, DC) Normal diet and no treatment. (Treatment control, TC) High fat, high sucrose diet (HFSD) plus saline vehicle. (Pravastatin, PR) HFSD plus pravastatin at 1.25 mg/kg/day. (Paroxetine, PA) HFSD plus paroxetine at 1.25 mg/kg/day. (Paroxetine and pravastatin, CO) HFSD plus paroxetine and pravastatin at 1.25 mg/kg/day for each drug. Animals were kept on their respective diets for 3 months prior to drug exposure. We measured 4-hour fasting blood glucose concentration after 3 weeks of drug treatment. Fasting glucoses were 68.5 ± 31.3 mg/dl (3.8 ± 1.7 mmol/l), 74.2 ± 26.7 mg/dl (4.1 ± 1.5 mmol/l), 94.4 ± 29.6 mg/dl (5.2 ± 1.6 mmol/l), 128.1 ± 31.3 mg/dl (7.1 ± 1.7 mmol/l), 193.1 ± 23.8 mg/dl (10.7 ± 1.3) for DC, PR, PA, TC, CO groups, respectively. We tested the interaction effect of pravastatin and paroxetine using an analysis of variance with covariates and interaction terms on the log transform of the fasting glucose measurements. We included diet as a covariate in addition to the pravastatin and paroxetine exposures and the interaction term. Our preliminary analysis shows a significant effect from diet (β = −0.19 ± 0.13, P = 0.004), pravastatin (β = −0.15 ± 0.13, P = 0.02), and the strongest effect from the interaction of paroxetine and pravastatin (β = 0.33 ± 0.18, P = 5.0 × 10−4). We assessed significance using an F test.