Idiots' Guide to The Biochemistry and Management of Ketosis

Ketosis is a disease of dry cows that shows up in fresh cows. Fundamentally, we have a situation where the cow is mobilizing body fat (condition) faster than the liver is able to metabolize it. In order for the liver to normally metabolize that fat, glucose is required. If glucose availability is limited due to inadequate substrate (mostly propionate from the diet) or glucose production via gluconeogenesis is inadequate or impaired, then ketosis can result because of the inability to convert the fat to energy.

     Loss/mobilization of body fat is a normal part of the onset of lactation. As the rate of fat mobilization rises, circulating NEFA levels begin to rise. If these fatty acids reach the liver and begin to accumulate in significant amounts, the liver switches away from TCA towards ketogenesis in an attempt to provide more energy and eliminate the fat buildup. Ketogenesis produces the ketone bodies, acetoacetate and beta-hydroxybutyrate. Some ketone production is normal in all periparturient cows, so diagnosis is made on clinical history, physical examination, and the presence of significant ketones in milk or urine. Presence of ketones in milk or urine is inadequate, in and or itself, to make the diagnosis of clinical ketosis.

     Feed intake, or lack thereof, is a critical component in the onset of ketosis. In all cows, dry matter intake begins to decline approximately one month prior to calving, although many people will not notice this decline until several days prior to calving. as feed intake declines and galactopoeisis begins, body fats are mobilized, resulting in an increase in circulationg NEFA levels. NEFAs themselves are mild appetite suppressants, so they continue to hamper feed intake. NEFAs are also the primary substrate for the production of ketone bodies via ketogenesis. Ketones are potent appetite suppressants, so an increase in their presence also decreases intake.

     So what we have is a prepartum cow with elevated levels of NEFAs and ketones, both acting to suppress appetitie, thus dry matter intake is declining. At the same time the growing fetus has increasing nutritional needs and is taking up increasingly more physical space within the abdominal cavity. It is easy to see that this is a downward spiral unless appropriate management is in place to provide and encourage consumption of an appropriately formulated ration in large quantities and in a comfortable environment.

     Once calving  occurs, milk production places significant pressure on the liver to supply large quantities of glucose which are required for lactose production in the milk synthesis process, as well as the normal glucose that is required for cellular metabolism. Part of that glucose is utilized as body fats are mobilized and converted back to a readily useable energy form by the liver. If liver funtion is impaired due to poor prepartum management, then ketosis may result, usually in the first several weeks of lactation. These cows often have a history consistent with adequate to excessive body condition at calving that is then lost very rapidly, often resulting in a significantly thinner cow at the time of physical examination. Producers may or may not notice poor appetities up until the time the clinical cow goes off feed. Often times, other peripartuient diseases will be either concurrent or noted in the history of animals that develop ketosis. Some clinicians will be able to smell ketones on the breath of affected cows. Approximately 85% of cows respond positively to a single IV dose of 500cc of 50% dextrose. Some practitioners may supplement this treatment with the use of insulin and vitamin B complex. Producers may follow up with drenches of propylene glycol or calcium propionate gels as necessary. While prevention is far preferable, getting affected cows back on feed as quickly as possible is the key to successful treatment.

     Some producers will ask about the use of monensin as a preventive. While theoretically this is sound based on the idea that monensin increases rumen propionate production and thus glucose precursors available for the liver, this practice is not allowed in the United States due to residue concerns and should be strictly avoided.

     Likewise the use of recombinant somatotropin has been postulated as an aid in the treatment of ketosis because of its gluconeogenic and glucose sparing effects on the body. While again based in sound biological theory, clinical evidence gathered to date shows no benefit to either rate or extent of productive recovery when clinicallly affected animals are treated with dextrose and somatotropin vs. the standard dextrose treatment alone. This would also represent an extra-label use, and is not allowed in animals intended for food production purposes.

Mike Lormore MS, DVM




Copyright 1999-2001
New Bolton Center Field Service Department
Students:  Keith Javic - Class of 2003, C. Nikki Conroy - Class of 2003