How is ketosis away from the eyes of livestock farmers? What is the cost of ketosis?
It is said to be a condition in an animal in which the concentration of ketone bodies (acetoacetate, beta-hydroxybutyrate and acetone) in the blood increases above a certain limit. This state is the result of the massive release of fatty acids from adipose tissue, which is more than the ability of the liver to completely oxidize all fatty acids. Therefore, the liver uses the ketogenesis pathway as a secondary way to get rid of excess fat. This condition usually occurs during the transition period and early breastfeeding.
Ketosis can exist in two clinical and subclinical forms. In clinical ketosis, the blood beta-hydroxybutyric acid level reaches 3 mmol/L or higher. But it is the subclinical form of ketosis that greatly compromises herd health, performance, and profitability. The definition of subclinical ketosis is usually defined as a state in which the blood beta-hydroxybutyric acid concentration is above 1.2 mmol/L without showing clinical symptoms. Many farmers do not know about the existence of ketosis in the herd. In fact, this is the reason for applying the term subclinical to this abnormality. Ketosis is caused by the animal’s inability to cope with a negative energy balance. This inability causes a series of metabolic changes that lead to the mobilization of body fat tissue for energy. does
Causes of ketosis
lack of energy
The main cause of ketosis is the lack of glucose in the body. Late in pregnancy, the body directs glucose to the growing calf, and when lactation begins, large amounts of glucose are needed for the synthesis of milk lactose and fat, although body stores are limited. A cow needs about 50 grams of glucose to produce 1 liter of milk with 4.8% lactose and 4% fat. If the diet does not have enough carbohydrates to meet the animal’s glucose needs, the cow’s body compensates for the lack of energy by using body fat and muscle tissue.
obesity
Cows with high efficiency and nutritional level are in the high risk group. The higher the cow’s body score at calving, the higher the probability of ketosis. Cows with a body score of 3 to 3.5 will be less likely to enter ketosis.
Improper nutrition
Ketosis is also often called a “starvation” disease – it is a disorder of protein, fat and carbohydrate metabolism in which the amount of ketone bodies in the body increases. Improper feed balance (carbohydrate deficiency), poor feed quality (e.g. low quality corn silage) are some of the factors that lead to ketosis. Cows should be fed with straw as much as possible during the dry season. If the straw is properly chopped and mixed well with the hay or corn silage, it usually helps. This disease often occurs not because the cow does not receive food, but because it is unable to absorb enough of it.
Genetics
Ketosis usually occurs in cows that are genetically predisposed to it.
Symptoms of ketosis
Ketosis can be shown in two ways:
A: Lack of energy
lethargy (head down, lack of energy)
Reduction of dry matter consumption
Decreased milk production
often sweet smell in breath (acetone)
B: Nervous form
Excitement, behavioral inconsistency and even aggressive moods
Strange behaviors such as eating dirt, licking fence posts and gates, walking in circles, or standing with heads up and…
The incidence of ketosis
McArt et al., studying 1717 cows in four large herds in the United States, reported a subclinical ketosis rate of 43%, which ranged from 26 to 56% in different herds, and found that new cases of subclinical ketosis immediately after It happens from childbirth and the highest rate of its occurrence was in 5 days after childbirth. Ketosis is considered as the starting point of problems and diseases.
Negative effects of ketosis on milk production
Ospina et al. (2010) reported that cows whose plasma beta-hydroxybutyric acid concentration was more than 1 mmol/L produced 7% less milk than other cows in 305 days of lactation.
McArt et al. (2012) reported that cows with subclinical ketosis produced 2.8 kg less milk in the first 30 days of lactation than healthy cows. Also, the same researchers in 2011 showed that early detection of ketosis and its treatment increased milk production by 2.3 kg compared to cows whose ketosis was not treated.
Increased probability of removal immediately after delivery
McArt et al. (2012) reported that cows with subclinical ketosis have a 3 times higher chance of being removed from the herd (due to death or sale) in the first 30 days after calving, and the more severe the ketosis, the more likely it is to be removed. increases in the same proportion, so that for every 0.1 unit increase in plasma beta-hydroxybutyrate concentration, the chance of removing cows from the herd increases 1.4 times.
Increase in the occurrence of breastfeeding
McArt et al. (2012) reported that the risk of mammary displacement in cows with subclinical ketosis was 19 times that of healthy cows. Also, these researchers reported that with the increase in severity of subclinical ketosis, the risk of mammary displacement also increases, so that for every 0.1 unit increase in plasma beta-hydroxybutyric acid concentration, the risk of mammary displacement increases by 1.1 times, so that cows with beta-hydroxybutyric acid concentration increase by 1.1 times. 2.4 mmol/L butyrate was 3.1 times more likely to develop udder displacement than cows with 1.2 mmol/L beta-hydroxybutyrate concentration.
Increased risk of metritis
Duffield et al. (2009) reported that increasing the concentration of beta-hydroxybutyrate in the first week of lactation to above 1.2 mmol/L increases the risk of metritis by 3.4 times. These researchers suggested that the dysfunction of the immune system resulting from ketosis could explain this effect. Ospina et al reported a 2.3-fold increase in the risk of metritis in cows with beta-hydroxybutyric acid concentrations higher than 0.7 mmol/L.
Decreased fertility
Ospina et al. (2010) studied larger herds in New York in the 2000s and reported that pregnancy tended to decrease in cows with β-hydroxybutyric acid above 1 mmol/L (p = 0.1) McArt et al. Colleagues (2012) investigated 4 large herds of dairy cows and reported a decrease in the pregnancy rate on the 150th day of lactation in cows suffering from ketosis in the first week of lactation.
Ketogenesis control in three stages
First step:
The control mechanism is first applied in adipose tissue. The liver can remove 30% of the free fatty acids that pass through it, and therefore, if the flow of free fatty acids is high, the flow of these substances to the liver increases significantly. Therefore, factors that affect the release of fatty acids from adipose tissue play an important role in controlling ketogenesis.
. The use of glucose precursors stimulates the process of gluconeogenesis and increases the concentration of glucose, which in turn can prevent the release of fatty acids from adipose tissue through insulin.
. Niacin can reduce the possibility of ketosis and fatty liver by stimulating the release of insulin as well as the mechanism dependent on the hydroxycarboxylic acid-2 (HCA2) receptor, which has an anti-lipolytic effect and suppresses the release of fatty acids and lipolysis from adipose tissue. to give
Second step:
After being harvested by the liver, fatty acids are activated after being converted into acyl-CoA and have two fates: either they are converted to carbon dioxide or ketone bodies during beta-oxidation, or they are esterified to triacylglycerol and phospholipid. become Carnitine palmitoyl transferase-1 (CPT-1) activity regulates the entry of long-chain acyl groups into mitochondria before the initiation of beta-oxidation. The activity of this enzyme is low in the state of satiety, when the oxidation of fatty acids is reduced, and it increases during starvation, when the oxidation of fatty acids is increased. In conditions where free fatty acids enter the liver with a low concentration, the fatty acids are almost completely esterified and converted to acylglycerol and transported out of the liver in the form of very low density lipoproteins (VLDL). But in the negative energy balance, the concentration of free fatty acids increases, and as a result, the inhibition of the carnitine palmitoyl transferase-1 enzyme is removed, and more acyl-CoA beta-oxidation becomes possible. These events are aggravated by a decrease in the ratio of insulin to glucagon. Therefore, beta-oxidation of free fatty acids is controlled by the entry pathway of carnitine palmitoyl transferase-1 (CPT-1) into mitochondria. Carnitine deficiency may occur in dairy cows, and therefore fatty acids may not enter mitochondria easily and beta-oxidation may be disturbed. Since the process of gluconeogenesis in the liver is dependent on the oxidation of fatty acids, the disturbance in the β-oxidation of fatty acids caused by carnitine deficiency causes hypoglycemia due to the reduction of the process of gluconeogenesis in the presence of high amounts of free fatty acids in the plasma, which leads to the accumulation of lipids and muscle weakness. to be Therefore, to prevent the accumulation of excess fat in the liver, the use of carnitine supplements in the diet of cows during the transition period can be useful.
The third step:
After being harvested by the liver and after being converted into activated acyl-CoA, fatty acids have two fates: either they are converted to ketone bodies during beta-oxidation to carbon dioxide, or they are esterified to triacylglycerol and phospholipid. . In the state of energy balance, free fatty acids that enter the liver at low concentrations are almost completely esterified and converted to acylglycerols and transported out of the liver in the form of very low density lipoproteins (VLDL). But with negative energy balance and hormonal changes, the concentration of free fatty acids increases.
. Choline helps to make lipoproteins in the liver and can remove fatty acids entered into the liver in the form of VLDL and prevent the development of fatty liver.
