|Hepatic Lipidosis in Dairy Cattle
Hepatic lipidosis, commonly referred to as “fatty
liver syndrome,” is a multifactorial syndrome of peri-parturient
dairy cows. It occurs most frequently in production situations
that commingle dry cows and lactating cows in a single group.
These cattle are likely to become over-conditioned late in
lactation or during their dry period. Mortality can be as
high as 25% without aggressive treatment and correction of
In over-conditioned cattle, fatty acids synthesized in
the liver are stored as triglycerides in adipose tissue at
extra-hepatic sites. With an increased energy demand not
met by a parallel increase in intake, triglycerides in adipose
tissue are converted to glycerol and NEFAs (non-estrified
fatty acids), which are bound to albumin in the blood. The
albumin bound NEFAs can be used as sources of energy by the
mammary glands, liver, spleen, and muscle. The liver receives
much of the NEFAs due to its large blood supply and efficiency
at extracting these substances. In the liver, NEFAs are re-estrified
back into triglycerides and remain in the liver until they
can be oxidized or repackaged in an envelope of cholesterol,
phospholipid, and protein. Repackaging and export from the
liver is a very slow process in cattle. Cattle with hepatic
lipidosis have smaller amounts of the packaging materials,
further slowing hepatic output. It is likely that glucose
availability influences the course of the disease, with high
glucose availability favoring fatty liver syndrome and the
opposite favoring ketosis.
Development of fatty liver syndrome can happen very quickly.
Triglycerides present can increase from 5% to more than 25%
in 48 hours under extreme conditions of fat mobilization.
A prepartum decline in DMI (Dry Matter Intake) appears to
increase the NEFAs in the serum at this time. This is most
severe in obese cows, those in stressful environments, or
those under nutritional stress. Endocrine changes that occur
at parturition may contribute to the decrease in DMI. It
has been shown that force-feeding to prevent a DMI drop will
reduce the amount of hepatic triglycerides accumulated at
day 1 postpartum.
Cows that develop fatty liver syndrome tend to be obese
or well-conditioned with high amounts of omental and/or subcutaneous
fat. They show nonspecific signs of illness, including depression,
anorexia, weight loss, and weakness that may lead to recumbency.
Decreased milk production and rumen motility are also evident.
Metritis, retained fetal membranes, mastitis, milk fever,
and displaced abomasum are some concurrent diseases that can
be present with fatty liver syndrome. The number of days
to first ovulation following calving has been shown to be
increased with greater amounts of triglycerides within the
Most diagnostic tests are poor indicators of hepatic lipidosis.
The most common clinical pathological abnormalities are ketonuria,
hypoglycemia, and increased serum free fatty acids. Liver
derived enzymes, such as GGT and AST, are usually higher than
in a dry cow, but are still within normal limits. Due to
decreased functional liver mass, the triglycerides and cholesterol
(mostly lipoproteins) may be decreased. Serum bile acids,
in one study, were found to be an unreliable indicator of
hepatic fatty degeneration.
A liver biopsy is the most accurate and reliable way to
confirm and assess the degree of fatty degeneration of the
liver antemortem. A mild to moderate amount of fat can be
present in the liver of most post-parturient high producing
dairy cows without evidence of disease. The amount of fatty
degeneration can be quantitated via histopathology or flotation
in copper sulfate solutions of varying specific gravities.
It has been shown that there is little correlation between
the amount of fatty degeneration and clinical signs until
it is marked and the liver will float in distilled water (SG=1).
On necropsy, fatty livers are usually yellow or tan.
Fatty degeneration is especially prominent in the centrilobular
and intermediate areas of hepatic lobules, and a pronounced
reticular pattern, on both serosal and cut surfaces, can usually
be observed. A white discoloration may be evident in the
abdominal fat due to accelerated lipolysis.
The main goal in treatment of fatty liver syndrome is
the elimination of the negative energy balance. This includes
administration of both glucose and insulin twice daily. Corticosteroids
can be used for treating the ketosis that may be present,
but only for a short period of time. Corticosteroids will
increase appetite, reduce milk production (to help alleviate
the demand for energy), and stimulate synthesis of glucose
from the stores present. Vitamin E and selenium have been
found to be low in cattle with fatty liver, and supplementation
is recommended. Transfaunation of rumen fluid from a normal
cow may increase production of volatile fatty acids used for
The best policy regarding fatty liver syndrome is prevention.
Goals of a good prevention program include the prevention
of obesity in cattle late in their lactation and during their
dry period. It is important to maintain a good breeding program
so that there are appropriate dry period lengths (45-60 days).
The ration should be balanced according to maintenance and
pregnancy requirements to maintain, not put on, condition.
At 2-4 weeks before calving, the grain content in the ration
should be slowly increased to acclimate the rumen flora to
the fresh cow ration.
Fatty liver syndrome can be prevented with proper management.
In situations in which management is poor, fatty livers, in
addition to the other problems mentioned, are likely to be
much more prevalent. With good management decisions, the
owner will be much happier with the efficiency and productivity
of the herd.
-by Lynne Catania, Class of 2002
-edited by Dr. Matt Renninger, VPB Graduate Student
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