Biomarkers of carbohydrate and lipid metabolism were evaluated in transition cows fed control (CON; n = 30) or SCFP (NutriTek, Diamond V, Cedar Rapids, IA; n = 34) TMR (45% NDF, 14% starch prepartum; 32% NDF, 19% starch postpartum) fed from −29 ± 5 to 42 d relative to calving. Blood samples were collected at the following time points relative to calving: d −28 to −24 (wk −4), d −14 to −10 (wk −2), d 3 to 7 (wk +1), d 12 to 16 (wk +2), and d 31 to 35 (wk +5). Plasma samples were analyzed for free fatty acids (FA), β-hydroxybutyrate (BHB), glucose, and insulin. Liver biopsies were taken once between d −19 and d −12 (wk −3) and at 14 DIM for analysis of liver triglyceride (TG) and cholesterol content and relative abundance of metabolic transcripts (FGF21, CPT1a, cPEPCK). Results were analyzed with repeated measures in a mixed model. Treatment did not affect plasma metabolites (FA, BHB, glucose, and insulin; all P > 0.35); mean FA concentrations (peak of 538 ± 42 μEq/L, wk 2) indicated a modest lipolytic rate. Relative mRNA abundance of CPT1a did not differ by treatment (P = 0.19); however, both cPEPCK and FGF21 tended to be greater for SCFP (P = 0.06 and 0.08, respectively). Liver TG increased from wk −3 to +2 (P < 0.001) but did not differ by treatment (P = 0.41). Liver cholesterol, in contrast, decreased from wk −3 to +2 (P < 0.001) and wk +2 liver TG and cholesterol concentrations were negatively correlated (R² = 0.18; P < 0.01). Liver cholesterol content tended to be lesser in SCFP than CON (P < 0.10). Despite a lack of treatment effect for plasma metabolites and no differences in BCS and BW, subclinical ketosis incidence (38% vs. 12%, diagnosed by daily urine ketone analysis) and days of glucogenic treatment (1.7 vs. 0.4 ± 0.3 d) were greater in SCFP than CON (both P ≤ 0.02). In conclusion, SCFP supplementation during the transition period did not alter plasma metabolites and only slightly affected cholesterol metabolism, but resulted in greater incidence of subclinical ketosis. Bioactive components of SCFP may have promoted ketogenesis in the absence of elevated NEFA supply.