Negative energy balance, subsequent rapid mobilization of triglycerides (TG), and accumulation of excess TG within the liver are characteristic of the transition to lactation period in dairy cattle. The objective of this study was to examine the coordinated response of hepatic lipolysis-associated proteins during the transition to lactation. Liver biopsies were collected at −14, +1, and +14 d relative to calving (DRTC) from multiparous cows. Liver TG were quantified and used to retrospectively assign cows to either a high (>20% liver lipids, dry matter; n = 5) or low (<20% liver lipids, dry matter; n = 3) treatment based on the maximal liver TG concentration. Protein abundance of hepatic abhydrolase domain containing 5 (ABHD5), hormone sensitive lipase (HSL), lipase A and C (LIPA, LIPC), lipoprotein lipase (LPL), perilipin 1 (PLIN), patatin-like phospholipase domain containing 2 and 3 (PNPLA2, PNPLA3) were determined through Western blot analysis and normalized to total lane protein. For analysis, each lipase was expressed relative to −14 DRTC and transformed as log(relative abundance +1) because data were not normally distributed. Data were analyzed for main effects of treatment, DRTC, and treatment × DRTC using PROC MIXED (SAS 9.4). Differences were declared at P < 0.1 and tendencies at P < 0.15. Cows with low liver TG had greater ABHD5 (P = 0.05) and HSL (P = 0.049), and tended to have greater LIPA (P = 0.146), LPL (P = 0.11), and PHSL (P = 0.12) abundance compared with cows with high liver lipids. Abundance of ABHD5 tended to be greater (P = 0.13) and PLIN was greater (P = 0.06) at +14 compared with −14 and +1 DRTC. Abundances of LIPA (P = 0.0006) and PNPLA3 (P = 0.04) were decreased at +1 and then increased by 3.3 and 1.8 times by +14 DRTC, respectively. These data indicate that cows with lower liver TG postpartum had a greater abundance of some hepatic lipases while other hepatic lipases are increased postpartum regardless of liver TG concentration. This suggests that there may be a coordinated response of several hepatic lipases to mediate both liver TG accumulation and subsequent remobilization during fatty liver recovery.