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Fatty Liver Syndrome

It is a metabolic disorder of excessive fat accumulation in the liver during periods of negative balance. This is in contrast to fat being deposited in adipose tissue during positive energy balance. The most common of negative energy balance is the periparturient period starting two weeks before parturition. This happens as absence of insufficient gluconeogenesis and energy intake. However, the relative magnitude of the negative energy in the dry period is small compared to that encountered during the first week after parturition.

In a dairy animal with a negative energy balance, fat is mobilized from adipose tissue stores, leading to increased blood concentrations of NEFA. The NEFA are taken up by the liver and can be oxidized to ketone bodies or carbon dioxide or can be esterified to triacylglycerols (TG). Fatty liver occurs when the rate of liver TG synthesis exceeds the rate of liver TG, disappearance through hydrolysis and export as part of very low density lipoproteins. Adipose tissue is the predominant fix lipogenesis in ruminants whereas in birds and human beings liver is the corresponding site.

During the periods of excessive fatty acid mobilization from adipose


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:
To 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 postpartum.

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.


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