Improving Liver Function Can Lead to Better Transitions
Transition cow health: get it right, cows peak well and breed back quickly. Get it wrong and cows may leave the herd before they even reach peak milk.
“The transition to lactation is the most metabolically challenging period in a cow’s life, but it also represents a period of great opportunity,” says Heather White, assistant professor of nutritional physiology at the University of Wisconsin. Transition is also the time when the cow’s liver is the most challenged. That’s because the demand for glucose and energy dramatically increases at the same time when feed intake declines. The result is a shortage of energy and glucose precursors. When the body tries to compensate, ketosis and fatty liver may occur.
Research has already shown the value of feeding a diet with negative DCAD (dietary cation-anion difference) to pre-fresh cows to improve calcium metabolism and reduce the incidence of clinical and subclinical hypocalcemia. Now, new research is zeroing in on hepatic (liver) function and what can be done to help the cow meet that increase in demand for glucose and energy and have a more successful transition to lactation.
Understanding Liver Function
In the big picture, the liver makes glucose; which, in turn, is used to make lactose to support milk production, explains White. During the transition to lactation, cows often experience a negative energy balance. To compensate, they mobilize stored body fat which is transported to the liver in the form of nonesterified fatty acids (NEFA) and glycerol. However, the liver does not have the capacity to completely oxidize all of the fatty acids being mobilized and turn them into energy.
The NEFAs that are not converted to energy are metabolized through alternate cellular pathways forming ketones or triglycerides. The result is often ketosis, fatty liver syndrome and cows that fail to reach their genetic potential for milk production and animal health.
In addition, the oxidation of fatty acids also produces reactive oxygen species which can accumulate at the cellular level and result in oxidative stress. While it is not yet known how much oxidative stress is too much for cows, research does show that oxidative stress is associated with decreased cellular function and inflammation in other species.
What the Research Shows
The liver’s ability to synthesize triglycerides increases during transition. But its ability to export those triglycerides as very low density lipoproteins (VLDL) does not. VLDLs can be used as fuel for other tissues, including the mammary gland. Without the ability to export more VLDL, fat accumulates in the liver.
Feeding rumen-protected choline (RPC) may help. Research shows that cows fed RPC during the transition to lactation have reduced concentration of liver triglycerides (Zom et al., 2011; Goselink et al., 2013). Cows supplemented with RPC have more choline to make a key component (phosphatidylcholine) that is limiting in VLDL assembly and export. This suggests that the decreased triglyceride levels in the liver are the result of increased VLDL export (Goselink et al., 2013).
Choline is also considered a methyl donor, along with methionine, betaine and folate. Research by Pinotti et al., 2002, showed that due to rumen fermentation, cows are deficient in methyl donors. Methyl donors are needed to make milk protein, build muscle, export fat from the liver as VLDL, and at the cellular level for DNA to properly function and for the regeneration of methionine. When methyl donors are in short supply, one or more of these pathways will be decreased.
Researchers at the University of Wisconsin used a bovine hepatocyte cell culture model to better understand methyl donors’ role in maintaining liver health and optimizing liver function during transition (Chandler et al., 2015; Chandler et al., 2016). Choline and methionine were both evaluated. Results showed:
- Increasing choline concentrations can increase VLDL export from the liver.
- The addition of choline tended to reduce oxidative stress.
- Methionine and choline have separate roles in the liver.
- The requirement for methionine needs to be met, either by dietary sources or through endogenous regeneration.
- Choline can be used to donate a methyl group for methionine regeneration and may support gluconeogenesis — creation of glucose in the liver.
Another area of research showing promise is feeding conjugated linoleic acid (CLA) to marginally depress milk fat production in early lactation. About 50% of the total energy used for milk production goes toward milk fat production. Temporarily depressing milk fat frees up energy for other body functions during a time of negative energy balance. When conjugated linoleic acid is removed from the diet, milk fat production quickly returns to normal. (CLA supplementation to dairy cows is not currently FDA approved in the U.S. except for research.)
White also suggests monitoring the prevalence of ketosis in the herd and promptly treating affected cows. Detecting and treating metabolic disorders is critical to enable cows to reach their genetic potential for milk production. For more on ketosis, please see "You Can Prevent Hyperketonemia," in the March issue of the Dairy Nutrition Plus newsletter.
“Any strategy that can improve the liver’s efficiency or nutrient utilization can have a positive effect on milk production and animal health during the transition period,” says White. Talk to your nutritionist about using these strategies to improve liver health and liver function in your cows. Doing so can lead to a better transition to lactation.