Idiots' Guide to The Biochemistry and Management of
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
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
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
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
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