What about hepatic function?

Fatty liver (hepatic steatosis) is the most frequent metabolic pathology for dairy cows and high producing sheep, goats, and buffalo. The incidence is higher for high genetic value animals, because of the high requirement of nutrients of the udder and the insulin resistance that most of them experience. Genetic selection favors the highest producing animals which have a great aptitude to lose weight in the first weeks of lactation to mobilize fatty acids and cover the udder requirements. Diets high in fat concentration for lactating cows and buffalo, high body condition score (BCS) at calving, and rumen acidosis during the transition period all increase the risk of hepatic steatosis. Difficulties in diagnosis (the need for hepatic biopsies and blood analyses) affect a precise calculation of fatty liver prevalence. The peak of incidence is surely in the first month of lactation, approximately in 50% of the animals. New research is showing that the accumulation of triglycerides (TAG) in the liver is a common sub-clinical pathology during the whole life of ruminants, especially those of higher genetic value.Starting from calving, the energy requirements for milk production are higher than the energy produced from the diet and the rumen fermentation (volatile fatty acids and metabolizable protein). The consequent reduction of insulin production causes the mobilization of fatty acids from lipid tissue. These non-esterified fatty acids (NEFA) are transported through the bloodstream into the liver to be oxidized and to produce energy. Carnitine-dependent enzymes (carnitine acyl-transferase I and II) transports NEFAs into the mitochondria. Fatty acids are converted into chemical energy (ATP) and part of them become in ketone bodies (BHBA, acetone, and acetoacetate) that return to the bloodstream. Metabolic ketosis is an excessive plasma concentration of ketone bodies: if BHBA are more than 10-12 mg/dl (or 1-1.2 mmol/L), the animal is affected by the sub-clinical pathology. If NEFA level is higher than the enzymatic transport ability, they are re-esterified and stored as triglycerides (TAG) in the liver: there is a connection between ketosis and hepatic steatosis. High plasma ketone bodies mean that too many fatty acids arrive at the liver with a high risk of accumulation into the hepatocytes.

Fatty liver is defined as a pathological concentration of TAG in this organ: hepatic biopsy or liver examination during the necropsy can easily diagnose this pathology. Physiological values are lower than 1% TAG, medium severity pathology is 1-10%, while it is severe if TAG concentration is higher than 10%. The evaluation of plasma NEFA and BCS measurement pre- and post-calving indicates fat mobilization and nutritional status. Milk fat is a good biomarker to evaluate the hepatic steatosis and metabolic ketosis risk. A fresh Holstein cow producing more than 4.8% fat milk is probably mobilizing high quantities of long-chain fatty acids from lipid tissue. The Fourier transform infrared spectroscopy (FTIR) uses the medium infrared spectra (MIR) to determine the different fatty acids in the milk in a cheap and fast way. By this method, we can assess which fatty acids derived from rumen fermentation (from C4:0 to C14:1, named de novo), from the diet (from C16:0 to C17:0, named mixed), and from both diet and body fat (C18:0, C18:1, and C18:2). Normally, milk fat is composed 18-30% by rumen fermentation fatty acids, 35-40% by the mixed ones, and 30-35% by the preformed fatty acids. The determination of NEFA origin is useful to individuate the risk factors and to prevent fatty liver.

Blood analysis can indicate fatty liver in single animals. GOT-AST, GPT-ALT, and SDH are biomarkers of hepatocytes integrity; bilirubin indicates the excretory function; AP-GGT indicates bilious integrity; urea, albumin, and total cholesterol indicate the hepatic function.

Excessive weight loss during the transition period and the wrong use of dietary lipids are important risk factors for hepatic steatosis. They are associated with endo-toxicosis (the passage of toxins to the bloodstream) caused by rumen Gram-negative bacteria death because of rumen acidosis (clinical or sub-clinical), mastitis, or metritis. Endo-toxins stimulate pro-inflammatory cytokines and reduce the available amount of lipoprotein that transfers TAG to the blood: the consequence is the accumulation of TAG in the hepatocytes.

In the case of hepatic steatosis, in the hepatocytes there is an accumulation of NEFA, BHBA, and acetoacetate, and the reduction of citrates and glycogen. Beta-oxidation and ketogenesis are reduced because of the reduction of the apo-protein B, protein-kinase B and C, and the carnitine palmitoyltransferase. Even if hepatic lipidosis is not severe, the animal produces fewer cholesterol esters and consequently lacks steroid hormones such as estrogen and progesterone. At the same time, there is a reduction of insulin and endotoxins clearance as well as gluconeogenesis. If lipids accumulate even in the pancreas, insulin and glucagon production are reduced. The reduced production of urea increases the risk of blood ammonia accumulation: the result is the inconsistency between blood and milk urea and the diet or the physiological phase of the animal. Utilizing urea nitrogen and plasma urea concentration analysis for the hepatic function is a tool available for monitoring.

The liver decreases IGF-1 production. This hormone stimulates the granulosa cells to produce estrogens and progesterone and improves follicular receptors’ response to LH stimulation. Fatty liver causes the reduction of ovary function and fertility performance due to the decrease in the production of sexual hormones, lower gluconeogenesis (low available energy), and altered hepatic detoxification of ammonia and toxins. At the same time, the immune system function is affected (lower cytotoxicity and phagocytosis ability, reduced production of immunoglobulins and interferon) with an increase in mastitis and metritis incidence. In the case of hepatic steatosis, the acute phase proteins are not correctly synthesized or degraded by the hepatocytes and their accumulation into the liver worsens the pathological status.


Fatty liver is a common pathology in high producing dairy ruminants. Correct hepatic function is necessary for productive, reproductive, and economic performance. Detailed management practices and nutrition with the use of specific feed additives, especially during the transition period, can mitigate the effect of the negative energy balance and improves animal performance.For more information: marketing@vetagro.comOriginal article here.