Carnitine palmitoyltransferase I in liver of periparturient dairy cows: effects of prepartum intake, postpartum induction of ketosis, and periparturient disorders.

Abstract Thirty-five multiparous Holstein cows were used to determine the role of mitochondrial carnitine palmitoyltransferase I (CPT I) in liver on peripartal adaptations of fatty acid metabolism. From dry-off to parturition, cows were fed a diet at either ad libitum (n=17) or restricted intake (RI, 80% of calculated requirements for net energy; n=18). After parturition, all cows were fed a lactation diet. At 4 d in milk (DIM), cows underwent a physical examination and were classified as healthy (n=15) or having at least one periparturient disorder (PD; n=17). Cows in the healthy group were assigned to either a control (n=6) group or a ketosis induction (KI; n=9) group. Cows with periparturient disorders were assigned to a third (PDC; n=17) group. Cows in control and PDC groups were fed for ad libitum intake. Cows in KI were fed at 50% of their respective intake at d 4 postpartum starting from 5 DIM and continuing to signs of clinical ketosis or until 14 DIM; cows then were returned to ad libitum intake. Liver was biopsied at −30 d, 1 d, at signs of clinical ketosis or 14 d, and 28 d relative to parturition. Mitochondria were isolated by differential centrifugation. Activity of CPT I was 5.4 and 7.6nmol of palmitoylcarnitine formed per min/mg of protein for ad libitum and RI, respectively, at −30 DIM. Sensitivity of CPT I to its inhibitor, malonyl CoA, did not differ between ad libitum and RI cows. Differences in CPT I activity between ad libitum and RI were no longer significant at 1 DIM. Postpartum CPT I activity and malonyl CoA sensitivity at 1 DIM, onset of clinical ketosis or 14 DIM, and 28 DIM were not affected by prepartum intake (ad libitum vs. RI), postpartum health status (healthy vs. PD), or ketosis induction status (control vs. KI vs. PDC). Activity of CPT I was positively correlated with liver total lipid, liver triglyceride, liver triglyceride to glycogen ratio, and serum nonesterified fatty acids. Activity of CPT I and dry matter intake were not correlated. Prepartum intake affected prepartum CPT I activity but not malonyl CoA sensitivity. Neither induction of primary ketosis nor periparturient disorders greatly affected CPT I activity or sensitivity, which indicates that alterations of CPT I may not be a major factor in the etiology of primary ketosis or other periparturient disorders.