tissue, insufficient lipoprotein synthesis may lead to hepatic
accumulation of TG i.e. development of fatty liver. Protein
nutrition may influence very low density lipoproteins (VLDL) of
synthesis and affect (TG) export from the liver. Estrogen,
especially estrone of placental origin, which is elevated in
gestation, has also been implicated in the development of fatty
liver. A fatty liver is a compromised liver and will not respond to
metabolic challenges as it should, resulting in impaired health,
fertility and milk production.
Dairy animal may experience negative energy balance in the dry
period if energy intake is less than demands for maintenance, foetal
growth, and organ metabolic changes in preparation for lactation.
Any kind of stress will aggravate the situation. Stressors that
lower feed intake can stimulate release of fatty acids into the
blood and be converted to storage fat in liver. Hormonal changes
around parturition, especially estrogen increase and decrease of
progesterone, trigger a dramatic increase in NEFA's, which
potentiate TG deposition in the liver. This is further enhanced by
adrenaline and noradrenaline release and hypophagia during calving.
Important by-products of fat metabolism for energy are ketones. Any
situation that leads fat
metabolism can result in fatty liver and ketosis.
Almost all dairy animals will have an increase in liver fat the day
after calving, but the major rise occurs between 2 weeks
before and 1 day after calving.
Once deposited in the liver, fat content does not diminish until
after the buffalo/cow returns to positive energy balance, and
is gaining weight. Typically, this occurs 5 to 12 weeks after
calving. During lactation, the
mammary gland becomes a deposit for fat being synthesized into milk
fat and protects the liver from fat accumulations.
Interrelationship Between Ketosis and Fatty Liver:
The occurrence of both these disorders is characterized by elevated
plasma NEFA concentrations, fat infiltration into the liver and
negative energy balance. Ketosis is caused by an inadequate
supply of glucose to meet
metabolic needs. When the diet and glycogenesis are insufficient to
meet the demand for glucose, fat is mobilized to provide
glycerol as a glucose precursor and meet energy demands of other
tissues. Fat mobilization may result in excessive fatty acid uptake
by the liver and production of ketones. Excessive fat accumulation
in the liver compromises
glycogenesis. If this results in enhanced levels of circulating
ketones, it may diminish appetite and feed intake. Glucose
output by the liver is then reduced even more. The low glucose
output will decrease insulin secretion and result in
increased lipid mobilization
creating a vicious cycle of events.
Guidelines to Diagnose Fatty Liver:
diagnose fatty liver in individual dairy animals, biopsies are taken
with a Tru-Cut biopsy instrument
via a stab incision over the 10th intercostal space at the
level of the greater trochanter and the biopsy needle is directed
towards the left elbow joint. Samples collected with this
instrument usually weigh 15 to 30
mg and can be divided into 2 or 3 subsamples. Samples are plunged
beneath the surface of the test liquid and observed for
floatation. A convenient and meaningful clinical test can be
performed using water and solutions of copper sulphate with specific
gravities of 1.025 and 1.055. Liver samples that float in all 3
liquids have fat concentrations in excess of 35 %. Those that sink
in water, but float in the other 2 liquids have levels greater than
25 %, but less than 35 % fat. Samples that float only in the
solution of 1.055 specific gravity have levels greater than 13 %,
but less than 25 % fat. These
liver fat concentrations are expressed on wet weight basis.
Clinical interpretation of liver
fat concentration is not a straight forward process. Buffaloes/cows
with hepatic concentration exceeding 35 % essentially have no
histologically normal liver tissue and will be clinically ill,
having a very poor prognosis
Animals with fat concentrations of 25 to 35 % often show clinical
signs, but not always. There is probably an interaction between
stress and liver fat concentration that determines whether or not
disease will develop. Animals with liver fat concentrations of 13 to
25 % often do not exhibit clinical signs but are at an increased
risk of disease, death and culling
compared to animals with less
than 13 % liver fat.
Prevention of Fatty Liver:
The energy gap in the pregnancy and early lactation should be kept
as small as possible by maximizing energy intake, in order to reduce
fatty acid mobilization from adipose tissue, and prevent excessive
depletion of hepatic glycogen. Strategies must be developed that
will minimize fatty acid mobilization from adipose tissue
decrease, esterification of fatty
acids in the liver, and increase export of TG as VLDL. This can be
achieved in various ways; maintain the maximum dry matter
intake prior to calving, this is very critical in minimizing
negative energy balance. Another
way to minimize negative energy balance is to increase the
energy density of the close-up diet by providing grains, up to a
maximum of 3 kg/cow, starting 2 to 3 weeks before the
expected calving date.
Elimination of stressors around calving helps maintain dry matter
intake in the periparturient period. Therefore, sudden changes in
diet ingredients, especially less palatable ingredients hould be
used with care. New fee ingredients should be introduced gradually.
Proper housing management is also important from stress point of
view. Environmental and group changes also will create stress on the
dairy animals and hey may go off feed for a while.
Drenching dairy animals with propylene glycol, especially animals
with a high body condition score, during the last 7 to 10 days
before calving may reduce fatty liver and ketosis but is very labour
intensive. Propylene glycol is converted to propionic acid in the
rumen which is converted to glucose by the liver and cause the
animal to have an insulin response. Insulin reduces fat mobilization
from storage depots and consequently reduces liver fat accumulation.
Labile protein reserves in dairy animals are limited relative to
lipid reserves. Underfeeding protein in late pregnancy may cause
depletion of material labile protein reserves, leading to extra
absorbable amino acids. Feeding more than 12-13% protein in the
close up period is correlated with decreased risk of retained
placenta and primary ketosis. Increasing dietary undegradable
protein may enhance utilization and undegradable protein
supplementation prepartum have a positive response on performance
Changes in body condition are positive indicators of energy balance.
Overconditioned animals eat less after calving and are more
susceptible to ketosis. An animal with a body condition score of 3.5
or less, probably would have greater appetite and fewer metabolic
problems after calving. Feeding for a targeted body condition at dry
off should begin at mid-lactation and continued through the
postpartum risk period.