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Dietary L-Carnitine Prevents Fat Accumulation In The Liver Of Transition Dairy Cows
by David B. Carlson, Joseph W. McFadden, Noah B. Litherland, and James K. Drackley


  • L-Carnitine is the naturally-occurring compound required for oxidation of long-chain nonesterified fatty acids (NEFA).
  • Previous research in our laboratory has demonstrated that postruminal infusion of L-carnitine reduced liver fat accumulation in feed-restricted lactating cows.
  • In transition dairy cows, dietary supplementation of L-carnitine (≥ 6 g per day) decreased liver fat concentration, which may reduce the risk of metabolic disorders and improve cow health.
  • Further research is required to develop a cost-effective, rumen-stable source of L-carnitine for use in dairy cow rations.


Fatty liver is a metabolic disorder that is strongly associated with an increased risk for ketosis, metritis, displaced abomasum, poor reproductive performance, and altered immune response. It has been reported that over 50% of dairy cows experience fatty liver to some degree, although the degree of fat accumulation and the true consequences of this disorder are difficult to quantify. However, it is clear that excessive liver fat accumulation can negatively impact production and health of dairy cows and alter the long-term profitability of the subsequent lactation.

Release of nonesterified fatty acids (NEFA) from fat stores is elevated around calving to support milk production during a time of depressed dry matter intake (DMI). Transition cows are prone to liver fat accumulation because NEFA uptake and esterification of NEFA to triglycerides (TG) often exceeds the liver’s capacity to oxidize NEFA and export TG. Carnitine is a naturally-occurring compound required for transport and subsequent oxidation of NEFA in the liver. Our previous research has shown that, during feed restriction (50% DMI for 5 days), carnitine reduced liver fat accumulation compared with feed-restricted cows not receiving carnitine. In fact, feed-restricted cows receiving carnitine produced more 3.5% fat-corrected milk than feed-restricted cows that did not receive carnitine. The objectives of this study were to test the effects of different levels of dietary carnitine on liver metabolism and milk production of transition dairy cows.


Forty-eight multiparous Holstein cows were assigned to the experiment on day 25 prior to expected calving date and were fed and monitored individually until day 56 in lactation. All cows were fed the same prepartum ration (12.7% CP; 0.68 mcal/lb NE L) from day -25 until calving, and the same postpartum ration (15.8% CP; 0.80 mcal/lb NE L) from calving until day 56 in lactation. The treatments were control (CON; no supplemental L-carnitine), low carnitine (LC; 6 g/d L-carnitine), medium carnitine (MC; 50 g/d L-carnitine), and high carnitine (HC; 100 g/d L-carnitine). Carnitine was mixed with corn (0.5 lb/d) and molasses (0.5 lb/d) and supplemented twice daily as a topdress from day -14 prior to expected calving until day 21 in lactation.

Dry matter intake was measured daily throughout the experiment. Milk yield was determined daily after calving, and milk samples were taken weekly from calving until day 56 in lactation. Liver biopsies were performed on day -21, +2, +10, and +28 relative to calving. Liver tissue was analyzed for concentrationsof total lipid, triglyceride, and glyocogen. Liver tissue slices were incubated in vitro with radiolabelled fatty acids to determine the influence of dietary carnitine on rates of fatty acid oxidation and esterification. Blood samples were obtained at several time-points around calving and analyzed for contents of NEFA, glucose, beta-hydroxybutyric acid (BHBA), and urea N.


All carnitine treatments significantly reduced postpartum liver lipid and triglyceride (Table 1) concentrations compared with the CON treatment. As little as 6 g/d of the rumen-degradable L-carnitine source was required to reduce fat accumulation in the liver. The MC and HC treatments increased in vitro fatty acid oxidation and reduced the proportion of fatty acids converted to triglycerides by liver slices.

Table 1. Effect of dietary L-carnitine on liver TG concentration in transition cows.

Liver TG, % CON LC MC HC
Day +2 3.90 2.49 1.28 0.64
Day +10 5.96 2.50 1.57 1.57
Day +28 3.42 1.14 1.45 0.80

Serum NEFA concentration did not differ among treatments. However, plasma BHBA was increased by MC and HC, which is in agreement with in vitro metabolism data in which carnitine increased conversion of fatty acids to ketone bodies instead of being stored as fat in the liver. Blood glucose was not altered by treatment, but urea N was lower in MC and HC cows during the prepartum and postpartum periods.

Prepartum DMI was not affected by carnitine supplementation, but the HC treatment decreased DMI compared with CON during weeks 1 and 2 of lactation. Lower DMI led to a trend for lower milk yield by cows fed HC in weeks 1-6. However, the LC and MC treatments did not alter DMI or milk yield compared with the CON treatment. The HC treatment perhaps had greater ruminal bypass than anticipated and negatively affected DMI and milk yield.

Milk fat percentage was higher in MC (4.37%) and HC (4.55%) cows compared with CON (4.0%) and LC (3.98%) treatments, perhaps because precursors for milk fat synthesis were available in the blood instead of being stored in the liver due to increased NEFA oxidation. Milk protein concentration was unaffected by treatment.

Dietary L-carnitine supplementation significantly reduced liver fat accumulation through increasing the capacity of the liver to oxidize NEFA. Further research will be conducted to identify the optimum level of L-carnitine for transition dairy cows.

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